GENERAL SURGERY

PAPER - 1

SMAHRT NOTES
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1) Classify wounds. Stages (Phases) of wound healing. Factors affecting wound healing [15, 12]
a. Factors influencing healing of wound [19, 16, 10, 09]
b. Classification and types of wounds [02]
Ans.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of
the structure and function.
Description Heals by
It is incised, clean wound without any tissue loss. Ex: Primary
Rank and Tidy wounds
Surgical Incisions Intention
Wakefield
Untidy Contaminated & a/w tissue loss due to: Crushing, Secondary
classification
wounds Tearing, Avulsion, Devitalised injury, Burns etc. Intention
Based on type  Closed wound – Ex: bruise, haematoma, blunt injury;
of wound  Open wound – Ex: abrasion, incised, lacerated, penetrating)
1. Superficial wound – involve only epidermis and dermal papillae.
2. Partial thickness wound – involve skin loss up to deep dermis.
Based on
3. Full thickness wound – involve loss of entire skin and subcutaneous tissue
thickness of
4. Deep wounds – extends into muscles or deeper structures.
the wound
5. Complicated wounds – involve injury to vessels or nerves.
6. Penetrating wound – penetrates into either natural cavities or organs.
Based on
 Simple wounds – Involve only one organ or tissue.
involvement
 Complex wounds – Involve mixed tissues
of structures
 Acute wounds – show signs of healing in < 4 weeks; Ex: surgical or traumatic or
Based on the burn wounds etc.
time elapsed  Chronic wounds – does NOT show signs of healing – Ex: diabetic foot, decubitus
ulcers etc.
1. – Elective, made under asepsis – Ex: hernioplasty, excisions,
Berard wound thyroidectomy, surgeries of brain, joints, heart and transplant
classification 2. – made during urgent or emergency case; Ex:
of surgical Appendicectomy, gastrojejunostomy, pancreatic and biliary surgeries.
wounds 3. – it refers to wounds made during trauma or acute
{based on the order inflammation – Ex: acute abdominal conditions
of Infectivity rate} 4. – refers to the wound with evidence of pus, necrotic tissue, faecal
contamination etc.
Stages of Wound Healing:
1) Stage of haematoma and inflammation
2) Stage of granulation tissue formation and organisation: Here due to fibroblastic activity, synthesis
of collagen and ground substance occurs
3) Stage of epithelialisation
4) Stage of scar formation and resorption
5) Stage of maturation
PHASES of Wound Healing:
Inflammatory Phase (Lag or Substrate or Exudative Phase) – lasts for 72 hours. Here haemostasis,
coagulation and chemotaxis occur
 Proliferative Phase (Collagen/Fibroblastic Phase): begins from 3rd day and lasts for 3-6 weeks.
There will be formation of granulation tissue and repair of the wound
Remodelling Phase (Maturation Phase) – begins at 6 weeks & lasts for 6 mon. to 1 or 2 years
Factors that influence Wound Healing:
 Factors which promote healing: �
 Healing is delayed by:
 Foreign bodies such as fragments of steel or glass
 Infections, Diabetes, Nutritional factors (Vit C & protein deficiency)
 Poor perfusion with arteriosclerosis
 Glucocorticoids (Diminish fibrosis & cause weakness of scar)
 Mechanical factors such as ↑ local pressure (wound dehiscence) &
 Type of tissue (Labile & stable tissues have better tissue regeneration, whereas
permanent tissues form only scar)
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1. Differences between hypertrophic scar and keloid scars [13, 07]

a. Keloid [21, 02]
b. Hypertrophic scar [15]
Ans.
 Mature scar is pale, acellular, softer, flat & contains type I collagen.
 Keloid is defined as an abnormal scar (with thick type III collagen)
that extends beyond the margin of the original wound
 Hypertrophic scar is defined as an abnormal widened scar (with thin
type III collagen) but confined within the margin of the original
wound

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2. Wound Healing by Secondary intention [04]
Ans.
Healing of Skin (Open) Wounds: It involves both epithelial regeneration & the formation of
connective tissue scar.
Healing by First intention Healing by Second Intention
Healing of a clean, uninfected surgical When injury produces extensive damage to skin, the
incision in the skin joined with surgical healing process in such cutaneous wound is referred
sutures is known as healing by primary to as healing by secondary union or by second
union or by first intention intention.

E.g., Large wounds, abscesses, ulceration & infarction

Seen with minimal injury to skin, where
edges of the wound are approximate
Healing is by regeneration
It involves small clot formation, minimal
necrotic debris, mild inflammatory response debris, more intense inflammatory response, & Wide
& minimal scar
Wound contraction is not seen
Outcome: Neat Linear scar is Formed
of parenchymal organs
Seen with Extensive injury to skin, where edges of the
wound are distant
Healing is by regeneration & fibrosis
It involves larger clot formation, greater necrotic
scar formation
Wound contraction occurs and is mediated by
myofibroblasts
Irregular contracted scar is formed
1) Define and Classify Ulcers. Discuss investigations & Treatment of Venous Ulcer [21]
a. Types of Ulcers [20]
Ans.
Definition of ulcer: An ulcer is a break in the continuity of the covering epithelium, either skin or
mucous membrane due to molecular death
Classification of ulcers
1. Spreading ulcer – edge is irregular; floor contain profuse purulent discharge
2. Callous (stationary) ulcer – chronic non-healing ulcer, floor contains
Clinical Classification pale unhealthy granulation tissue; nontender edge; Ulcer does not show
any tendency to heal
3. Healing ulcer – Edge is sloping with healthy pink/red healthy granulation
tissue; minimal serous discharge in the floor
4. Non-healing ulcer – floor contains unhealthy
granulation tissue; here edge will be depending on
the cause:
Punched out – trophic ulcer
Undermined – tuberculous ulcer
Rolled out – carcinomatous ulcer
Beaded – Rodent ulcer
1. Acute ulcer – duration is less than 2 weeks.
Based on Duration
2. Chronic ulcer – duration is more than 2 weeks
1. Specific ulcers: Tuberculous; syphilitic; actinomycosis & Meleney's ulcer
2. Malignant ulcers: Carcinomatous; rodent (BCC); melanotic.
3. Non-specific ulcers – Ex:
Traumatic ulcer. It may be mechanical, physical, chemical-common
Pathological Arterial ulcer: Atherosclerosis
Classification Trophic ulcer/Pressure sore.
Tropical ulcers – It occurs in tropical countries. It is callous type of
ulcer, e.g., Vincent's ulcer.
Ulcers due to chilblains and frostbite (cryopathic ulcer).
Diabetic ulcer.

: It is common around ankle (gaiters zone) due to ambulatory chronic venous hypertension
: It is due to varicose veins (long saphenous vein/short saphenous vein/perforators) or post-
phlebitic limb
: females, (similar to varicose veins)
:
Venous ulcer is vertically oval with sloping edge and will not penetrate deep fascia
Floor is covered with pale or often without any granulation tissue
Ulcer is initially painful; but once chronicity develops it becomes painless
Complications: Scarring is common due to repeated healing and recurrent ulcer formation 
squamous cell carcinoma (Marjolin's ulcer).
:
 Study of discharge: Culture and sensitivity, AFB study, cytology.
Wedge biopsy: Biopsy is taken from the edge
X-ray of the part to look for periostitis/osteomyelitis
FNAC of the lymph node
Chest X-ray, Mantoux test in suspected case of tuberculous ulcer
Venous Doppler
:
Cause should be found and treated
Correction of the anaemia, deficiencies like of protein and vitamins
Control the pain and infection
Rest, immobilization, elevation, avoidance of repeated trauma
Care of the ulcer: debridement, regular dressing & skin grafting.
Normal saline is ideal for ulcer cleaning
Topical antibiotics for infected ulcers – Ex: mupirocin
Maggot debridement therapy – can inhibit many bacteria including MRSA & can increase the
granulation tissue formation also
Once ulcer granulates, defect is closed with secondary suturing, skin graft or flaps
Specific treatment for varicose veins
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1. Trophic ulcer [11, 04]

Ans.
(Pressure sore/ Decubitus ulcer)
It refers to tissue necrosis & penetrating ulcer due to prolonged pressure on the blood vessels
between bony prominence and skin.
Etiology:
 Nutritional deficiencies worsen the necrosis
 Inadequate padding over the bony prominences in malnourished patients
 Normal stimulus to relieve the pressure is absent in anaesthetised patient
 Urinary incontinence in paraplegia patient causes skin soiling-maceration-infection-necrosis
 Neurological causes �
Due to the presence of neurological deficit, trophic ulcer is also
called as neurogenic ulcer / neuropathic ulcer
Sites: Over the ischial tuberosity; sacrum; heel; heads of
metatarsals; buttocks; shoulder; occiput
Investigations: Study of discharge; blood sugar; wedge biopsy from the edge; X ray of the part and
spine
Treatment:
Treat the cause – Ex: correction of diabetes, anaemia etc.
Nutritional supplementation & Abx
Care of the ulcer: slough excision, regular dressings, Vacuum-assisted closure (VAC) etc.
Regular skin observation; Urinary and faecal care; hygiene; psychological counselling
Change in position once in 2 hours; lifting the limb upwards for 10 seconds once in 10 minutes.
Use of water bed/air bed/air-fluid flotation bed and pressure dispersion cushions to the affected
area
 Once ulcer granulates well, flap cover or skin grafting can be done
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2. Tuberculous Ulcer [04]
Ans.
It is due to Mycobacterium tuberculosis.
: Cold abscess  ulcer in the neck, chest wall, axilla and groin.
It can also be primary tuberculosis of the skin (commonly in face).
:
 Ulcer can be single or multiple; oval or rounded; with undermined edge (due to progression of
disease outwards underneath and healing inwards by skin), painless with caseating material on the
floor.
 Regional lymph nodes may be enlarged matted, firm, and nontender
: Discharge study for epithelioid cells (modified histiocytes), AFB; edge biopsy, ATT
drugs
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3. Chronic Non-specific ulcer [05]
Ans.

Features of Chronic Non-specific ulcer:

 Floor contains pale unhealthy, flabby, whitish yellow
granulation tissue with indurated nontender edge;
 Base is indurated, nontender and often fixed.
 Ulcer does not show any tendency to heal. It lasts for many
months to years.
 Tissue destruction is more.
 Regional lymph nodes may be enlarged & are non-tender.

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1. Marjolin's ulcer [19, 13, 09]

Ans.
It is a slow growing ulcer – seen in aggressive squamous cell carcinoma
Predisposing Factors: chronic wounds; burn injuries; varicose veins; post-radiotherapy scars etc.
Features: everted edges & painless ulcer; it doesn’t spread to lymphatics
Management: Wedge biopsy; Local Excision & Grafting
1. Branchial Cyst [12, 11, 04]
a. Branchial Fistula [06, 03]
Ans.

Definition: It occurs as a result of an abnormal development of primitive ectodermal pharyngeal

pouches and/ or the endoderm of the embryonic cervical sinus.
Site: Above or Below the hyoid bone
Second Branchial Arch Anomalies are most common. They can present as cyst, sinus, or fistula
Pathology: The cyst is lined
by stratified squamous Symptoms Signs
epithelium & contains Swelling is smooth, round, fluctuant, non-
Cholesterol Crystals • Painless tender & non-transilluminant
swelling in Swelling can’t be reduced or compressed.
Clinical Features: �
upper & lateral Fluctuation test – positive
Investigations:
part of neck. Present deep to the upper third of anterior
 Contrast X-ray
• Painful ↑ in border of SCM
(fistulogram) size at the time Branchial sinus. If present, may exude
 FNAC – cholesterol of URTI can mucoid discharge.
crystals (+) occur When both internal and external openings
Complications: Recurrent are present, it is called a branchial fistula
infections & acquired
branchial fistula
Treatment: Complete excision of the cyst or fistula from the neck to the pharynx is the treatment of
choice. It can be accomplished by step-ladder incisions
Differential Diagnosis: Submandibular salivary gland swelling, Plunging ranula, Cervical dermoid, Cystic
hygroma & Cervical lymph node
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1. Preauricular sinus [08]

Ans.
Definition: It is a congenital entity occurring due to imperfect fusion of the six tubercles which
form ear cartilage
Site: Sinus opening may be seen at the root of the helix or on the tragus
Clinical Presentation: cosmetic problem; Pain & discharge due to 2° infection
DDx: Cold abscess, sebaceous cyst
Investigations: Discharge study, ESR & sinusogram to assess the track
Treatment: Excision under general anaesthesia with removal of entire track to avoid recurrences
Preauricular sinus never communicate with the external auditory meatus
1. Dentigerous cyst [13, 94]
Ans.
Dentigerous Cyst (Follicular Odontome): It is a unilocular cystic swelling arising in relation to the dental
epithelium from an unerupted tooth. It leads to expansion of outer table of the mandible
 Sites: Lower jaw > Upper jaw. Commonly seen in relation to premolars or molars.
 Clinical feature: Pain less swelling in the jaw which is smooth and hard.
 Differential diagnosis: Adamantinoma; Dental cyst; Osteoclastoma
 Complication: It can turn into Adamantinoma.
 Investigation: Orthopantomogram – well-defined tooth within the cyst.
 Treatment:
 If it is small, excision of the cyst is done.
 If it is large, initial marsupialisation and later excision is done.
 Unerupted tooth should be extracted.
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2. Adamantinoma [10, 01, 92]
a. Ameloblastoma of the mandible [95]
Ans.
Ameloblastoma (Adamantinoma, Eve's Disease, Multilocular Cystic Disease of the Jaw):
It arises from the dental epithelium probably from the enamel/ dental lamina.
: 4-5th decades; Males
: mandible (5:1) or maxilla. Occasionally, it is seen in the base of the skull in relation to Rathke's pouch or in tibia.
: It is a locally malignant tumour. Histologically, it is a variant of basal cell carcinoma.
It neither spreads through lymph node nor through blood. Hence it is curable.
On microscopy  cords of odontogenic epithelium, connective tissue, stellate reticulum like
cells with columnar ameloblast like cells are seen
: “Swelling in the jaw” near the angle of mandible extending to vertical ramus
 Swelling is gradually progressive & painless with intact inner table (enlarges externally).
 Outer table expansion seen
 a/w eggshell crackling
 Lymph nodes are not enlarged.
:
 Osteoclastoma of the mandible – Here inner table is not intact.
 Dentigerous cyst; Dental abscess.,
 Giant cell reparative granuloma (Jaffe's tumour) – It is a swelling which occurs due to haemorrhage
within the bone marrow. It contains vascular stroma, collagen and connective tissue cells.
 Clinical presentation: FEMALES with painless enlargement of jaw.
 Treatment: calcitonin (100 units/0.5 mg subcutaneously daily for 12 months) or surgical curettage.
:
 Orthopantomogram (OPG) shows multiloculated lesion – Honeycomb appearance.
 CT scan of the region.
 Biopsy from the swelling.
 : Segmental resection of the mandible or Hemimandibulectomy with reconstruction of
the mandible.
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3. Cleft palate [03]
Ans.
The defective fusion of various segments of palate gives rise to clefts in the palate.
Etiology:
Familial – more common in cleft lip or combined cleft lip and palate (Risk is 1 :25 live births).
Chromosomal abnormalities.
Maternal epilepsy and drug intake during pregnancy (steroids/ eptoin/diazepam).
Protein and vitamin deficiency.
Rubella infection; Radiation.
Types of Cleft Palate: Unilateral Complete cleft Bilateral complete cleft
: It palate palate
can be U/L or B/L. � It occurs if maxillary
It occurs if both the maxillary
process on one side does
Cause processes fail to fuse with the
: These can be not fuse with the
premaxilla
premaxilla
of the following types:
 Bifid uvula – Cleft It is always Anterior V-
a/w cleft lip shaped cleft
involving only uvula.
Features on the same separate the
It is of no clinical premaxilla
side
importance. completely
 Cleft of the soft
palate: Involving uvula and adjoining part of the soft palate.
 Cleft of the soft palate extending into hard palate: Involving uvula, whole of the soft palate,
and extends into the hard
palate
Complications of Cleft Palate:
• Speech is defective especially in
cleft palate, mainly to phonate B,
D, K, P, T and G
• Bacterial contamination of upper
respiratory tract with recurrent
infection
• Small maxilla with crowded teeth, absent/poorly developed upper lateral incisors
• Chronic otitis media with deafness may occur
• Swallowing difficulties to certain extent and speech problems
• Cosmetic problems (Hypoplasia of Maxilla)
Treatment of Cleft Palate:
: 10 kg weight; 10 g% hemoglobin & 10 months of age (10-18
months).
: V-Y Palatoplasty
 Mucoperiosteum flap is raised
 Palatal defect is closed using 3 layers – nasal, muscle and oral layers
  Hook of pterygoid hamulus is fractured to relax tensor palate muscle to relieve tension on
suture line
 In Post-op period: Start speech therapy & regular examination of ENT during follow-up

Control of otitis media

Hearing aids (if defect is present)
Pharyngoplasty or veloplasty or speech devices – for speech problems
Dental Reconstructive surgery – for dental problems
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1) Frey's Syndrome [21]

Ans. Frey's Syndrome (Auriculotemporal Syndrome, Gustatory Sweating):
Etiology: Surgeries or accidental injuries to the parotid or TMJ
Pathogenesis: Injury to the auriculotemporal nerve (contain parasympathetic, sensory &
sympathetic fibres)  During regeneration, the parasympathetic fibres grow into endoneural
sheaths of fibres supplying cutaneous receptors for pain, touch and temperature, and sympathetic
fibres supplying sweat glands and blood vessels.
Clinical Presentation: Flushing, sweating, erythema, pain and hyperaesthesia in the skin over the
face innervated by the auriculotemporal nerve, whenever salivation is stimulated (Ex: during
mastication).
Investigation: Minor's Starch iodine test – Involved skin is painted with iodine and dried. Dry starch
applied over this area will become blue due to more sweat in the area
Treatment:
 Reassurance to the patient
 Conservative Mx:
 Antiperspirants, anticholinergics like scopolamine 3%, glycopyrrolate 1 % etc. can be used
 Most often, they recover within 6 months
 Occasionally (10% cases) require surgery  Jacobsen neurectomy (tympanic br. of IX nerve)
 Injection of botulinum toxin or alcohol to the affected skin can be tried.
 Precautions to be taken during parotidectomy to avoid Frey’s Syndrome: place muscle
(sternomastoid) or fascial (temporalis) flaps or artificial membranes over parotid bed, under the skin
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2) Cleft Lip [10, 05, 02]
Ans.
 Etiology – (same as Cleft Palate – refer 2nd SQ)
 Types of Cleft Lip – 3
: It occurs due to failure of fusion of maxillary
process with the medial nasal process of the same side.
: It occurs due to failure of fusion of maxillary
processes with the frontonasal process.
: It occurs due to failure of development
of philtrum of the upper lip from the frontonasal process. Very
rarely the two mandibular processes may fail to fuse in the midline to cause cleft lower lip.
 Treatment for Cleft Lip:
 – pounds weight; weeks old; g% hemoglobin.
 Millard cleft lip repair by rotating the local nasolabial
flaps
 Tenninson's 'Z' plasty (Tennison-Randall triangular flap)
can also be tried
 Proper post-op Mx like control of infection, training for sucking, swallowing and speech.
 Mx of associated cleft palate deformity
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3) Epulis [01, 2000]
Ans.
• Swelling arising from the mucoperiosteum of gums (gingiva) is known as Epulis
• Types of Epulis: Congenital epulis, Fibrous epulis, Pregnancy epulis, Giant cell epulis, Myelomatous
epulis, Granulomatous epulis, Sarcomatous epulis, Carcinomatous epulis etc.
• Treatment: Excision
 Pregnancy epulis resolves after delivery
 Myelomatous epulis respond to leukemia therapy
1. Describe the pathology, C/F & Mx of carcinoma of tongue [2000, 99, 94]
Ans.
 Age & Sex: men in the age group of 50–70 years.
 Majority are squamous cell type.
 Site: lateral border or the ventral aspect (MC), the tip or the dorsum of the tongue.
 Spread: Locally, it may infiltrate the lingual musculature causing ankyloglossia or may spread to the
floor of mouth & mandible.
- Lymph node metastases go to the submandibular and upper jugular nodes (from the lateral border
of tongue) and to the submental and jugulo-omohyoid group (from the tip).
 Clinical Features:
Signs Symptoms
Cancer of the tongue may present as 1) A lump in the mouth
a) An exophytic lesion like a papilloma 2) Early lesions are painless (hence asymptomatic for a long time).
b) A non-healing ulcer with rolled 3) Pain in the tongue occurs at the site of ulcer.
edges, greyish white shaggy base 4) Pain in the ipsilateral ear; it is due to common nerve supply of the
and induration tongue (lingual nerve) and ear (auriculo-temporal) from V3.
c) A submucous nodule with 5) Enlarged lymph node mass in the neck.
induration of the surrounding 6) Dysphagia, difficulty to protrude the tongue, slurred
tissue. speech and bleeding from the mouth are late features.
 Staging - TNM classification is used.
 Treatment.
- Small tumours give equal results if treated with radiotherapy or surgery.
- Stage III or IV tumours: Surgery + post-op radiotherapy.
- Depending on the size & extent, surgery may consist of hemiglossectomy
including a portion of the floor of mouth, hemimandibulectomy and block
dissection of neck nodes—the so-called “commando operation.”
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1) Leukoplakia - aetiology, clinical features and management [21, 14, 09]

Ans.
W.H.O. defined leukoplakia as a clinical white patch that cannot be characterized clinically or pathologically
as any other disease.
Risk factors:
Age and sex – mostly occur in 4th decade, Males > Females
Smoking, tobacco chewing, alcohol abuse.
Chronic trauma due to ill-fitting dentures or cheek bites.
It may also be a/w submucous fibrosis, hyperplastic candidiasis or Plummer–Vinson syndrome.
Sites involved- Buccal mucosa and oral commissures are the most common sites. It can also involve
floor of mouth, tongue, gingivobuccal sulcus and the mucosal surface of lip.
Clinical types
 Homogenous variety presents as a white patch. It is less often
a/w malignancy.
Nodular (speckled) variety presents as nodules on erythematous
base.
Erosive (erythroleukoplakia) variety – here leukoplakia is
interspersed with erythroplakia and has erosions and fissures.
Histology & Malignant Potential: About 25% of leukoplakias may
show some form of epithelial dysplasia. Higher the grade of
dysplasia more are the chances of its going into malignant
change. On an average about 5% become malignant
Management
Many of the lesions will disappear spontaneously if causative agent is removed.
Biopsy is taken to rule out malignancy.
In Suspicious lesions, surgical excision or ablation with laser or cryotherapy can be done.
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2) Premalignant conditions of buccal mucosa [15]
a. Premalignant conditions of oral malignancy [02]
Ans.
is a chronic process
in which juxtaepithelial deposition of fibrous
tissue occur in the oral cavity and pharynx – seen
in areca nut chewing {Paan, Betel quid}Trismus.
– {refer 1st SQ}
– aka Plummer-Vinson
syndrome
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3) Ranula [14, 11, 10, 06, 03, 02]
a. Plunging Ranula [19]
Ans.
Ranula looks like belly of frog, hence the name.
 Ranula is a cystic translucent swelling of Sublingual Salivary Gland due to
obstruction of its ducts
 Site: Floor of mouth on one side of the frenulum and pushing the tongue up.
 Usually appears as Blue
 Plunging ranula: Ranula often extends into the submandibular region through the deeper part of
the posterior margin of mylohyoid muscle and is called as plunging ranula.
- It is intraoral ranula with cervical extension presenting as soft, fluctuant, non-tender, dumbbell-
shaped swelling in the submandibular region.
- It is bi-digitally palpable
 DDx: Lymph cyst; sublingual dermoid etc.
 Investigations: US neck or MRI neck and oral cavity
 Treatment is complete surgical excision if small, or marsupialization, if large.
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4) Tumours of the Gums [05]
a. Carcinoma Cheek [03]
Ans.

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5) Haemangioma tongue [04]
Ans.
 It’s a vascular malformation of the tongue develop due to endothelial cell proliferation.
 They are rare lesions which can cause distressing problem to the patients, producing cosmetic
deformity, recurrent hemorrhage, and functional problems with speaking, mastication &
deglutition.
 Management:
 Identify the feeding vessel  intra-arterial embolization and surgical resection
 For superficial lesions: Direct puncture  inject Sclerosing agent (absolute ethanol).
1. Describe the classification of salivary gland tumors. Describe Pleomorphic adenoma – etiology,
pathology, C/F, inv. & Mx. Mention 4 complications of parotid gland surgery [19, 18, 09, 07, 02]
a. Mixed parotid tumor [16, 10, 97]
Ans.

Pleomorphic adenoma is a Benign tumor of salivary glands. MC salivary gland tumor.

It is aka .
{mixture of epithelial & mesenchymal elements}

 Site: Parotid (MC) > submandibular glands > sublingual gland

 Risk factor: Elderly Female, Radiation exposure etc.
 Genetic alterations: Overexpression of PLAG-1
{Pleomorphic Adenoma gene 1} ↑ cell growth
 C/P: Painless slow-growing & mobile mass at the
angle of the jaw.
 Pain can occur due to obstruction to free flow of
saliva or Nerve infiltration or Capsular distension
by tumour etc.
 Complications: Rarely may transform into carcinoma, which presents with signs of facial nerve
damage (facial nerve runs through parotid gland)
 Management
:
FNAC reveals mixture of epithelial & mesenchymal {cartilage-blue} elements {mixed tumor}.
CT scan/MRI to know the status of deep lobe, local extension and spread.
: Surgery- first line treatment
 Superficial parotidectomy – if only superficial lobe is involved
 Total conservative parotidectomy (by retaining facial nerve) – if both the lobes are involved
Extension of small islands of tumor through the capsule often leads to incomplete resection 
High rate of recurrence
----------------------------------------------------------------------------------------------------------------------------------------

1) Submandibular gland calculus [17, 04]

a. Submandibular sialadenitis [01]
Ans.
Sialadenitis is inflammation of the salivary gland

 Pain, swelling, tenderness is seen in

 Bacterial infection – due to ductal submandibular region & floor of mouth
Acute obstruction (Wharton's) or in parotid  Dysphagia, trismus, fever.
sialadenitis gland.  Double chin appearance due to
 Viral-mumps {Paramyxovirus) spreading of oedema downwards.
 Duct is inflamed and swollen.
 Pain & swelling is more during
 Stones in submandibular gland or
mastication due to stimulation;
hilum proximal to the crossing of the
Chronic  Size of the swelling will decrease again
lingual nerve over the duct
sialadenitis 2 hours after meal
 Partial obstruction of submandibular
 Kuttner tumour is chronic sclerosing
gland duct
sialadenitis of submandibular salivary gland
:
 Intraoral X-ray (dental occlusion films) to see radio-opaque stones (80%);
 FNAC of the gland to rule out other pathology;
 Total count and ESR in acute phase;
 USG will demonstrate stone with posterior acoustic shadow.
 CT scan head and neck may be occasionally needed to identify the features of the diseased
submandibular salivary gland
: Submandibular lymphadenitis; salivary neoplasm.

– Antibiotics & anti-inflammatory drugs.

:
Stones <4 mm are removed using sialendoscopy under local anaesthesia under USG guidance.
Use Pneumatic lithotripter for larger stones.
If stone is in the Wharton's duct anterior to the crossing of the lingual nerve, it is removed by
incising the duct under local anaesthesia
If stone is in the Wharton's duct behind the crossing of the lingual nerve it should be removed
using intraoral approach under general anaesthesia
In case of deep-seated stones in the duct which are not palpable – Surgical excision of
submandibular salivary gland
Calculi are common in submandibular salivary gland,
because:
 Viscous nature and mucin content
 More Calcium content.
 Non-dependent drainage, causing stasis
 Hooking of nerve by submandibular duct
----------------------------------------------------------------------------------------------------------------------------------------
2) Warthin tumour [13, 05, 04, 03]
Ans.
“Benign tumor of Parotid glands.”
 2nd MC salivary gland tumor.
 It’s a benign cystic tumor with abundant lymphocytes and germinal centers (lymph node-like
stroma; aka Adenolymphoma; Papillary Cystadenoma Lymphomatosum)
 It is a misnomer. It is not malignant, it is not lymphoma
Site: Parotid gland (exclusively)
Risk factor: Elderly Male; Smoking & Tobacco; It is the only salivary glands tumor that is more
common in males than in females
C/P: slow growing, smooth, soft, cystic, fluctuant swelling in front of & below the ear
Investigations:
 Adenolymphoma produces a "hot spot' in 99Technetium pertechnetate scan-it is diagnostic (Due
to high mitochondrial content);
 FNAC – reveals double layered epithelium & subepithelial dense lymphoid stroma
Treatment: Superficial parotidectomy
----------------------------------------------------------------------------------------------------------------------------------------
3) Parotid fistula [04, 88]
Ans.
Parotid fistula may arise from parotid gland or duct or
ductules.
It may open inside the mouth as internal fistula; or
open outside onto the skin as external fistula.
:�
:
Discharging fistula in the parotid region of the face, and discharge is more during eating
Fistula from the duct has profuse discharge. Fistula from the gland often shows only minimal
discharge
Tenderness and induration; Trismus
:
Sialography to find out the origin of the fistula whether from parotid gland or duct or ductules;
Fistulogram or CT fistulogram;
Discharge study;
MRI.
:
1. Anticholinergics – hyoscine bromide.
2. Radiotherapy.
3. Excision of fistula, repair of the duct, diversion of the duct into the mouth are other options.
4. Papillotomy – If there is stenosis at the orifice of the Stenson's duct
5. If still persists  cut auriculotemporal nerve which supplies secretomotor fibres to parotid
6. Total conservative parotidectomy is done in failed cases
1. Describe the D.D. of enlargement of cervical lymph nodes of 3 months duration. Describe T.B.
Lymphadenitis of neck – etiopath, C/F & Mx [21, 77, 73]
a. Tubercular Lymphadenitis [21]
b. Cold Abscess Neck [19, 11, 08]
c. Tuberculous cervical adenitis [06]
d. Lymph nodes in the neck [05]
e. Secondary Lymph node neck [03]
Ans.
:
Earlier called as Scrofula
It is the commonest form of
extrapulmonary tuberculosis.
:
Causative organism:
Mycobacterium tuberculosis
Mode of Infection: tonsils > lungs
MC in jugulodigastric LN
Stages �
It can be a/w HIV & lymphomas

Swelling in the neck which is firm, matted

Cold abscess is soft, smooth, nontender, fluctuant, without involvement of
the skin. It is NOT warm
As a result of pressure, cold abscess ruptures out of the deep fascia to
form collar stud abscess which is adherent to the overlying skin
Once collar stud abscess bursts open, discharging sinus (caseating cheesy
discharge) is formed.
Examine tonsils & cervical spine
:
 Ultrasound neck
 FNAC of lymph node and smear for AFB and culture
 HIV test (ELISA and Western blot), CD4 count
 Chest X-ray to look for pulmonary tuberculosis
 Treat with ATT Zig-zag' aspiration of cold abscess If it
recurs, then a nondependent incision & drainage  if
there is no response, then Surgical removal of diseased
lymph nodes + Excision of the sinus track
----------------------------------------------------------------------------------------------------------------------------------------

1) Ludwig's angina [08, 02, 97]

Ans. Ludwig’s angina is infection of submandibular space (It lies between mucous membrane of the floor of mouth and
superficial layer of deep cervical fascia extending between the hyoid bone and mandible on the other).
AETIOLOGY
1. Causative organisms: α-haemolytic Streptococci, Staphylococci and bacteroides are common. Rarely
Haemophilus influenzae, E. coli & Pseudomonas
2. Dental Infections – esp. premolar & molar teeth.
3. Submandibular Sialadenitis, Injuries of Oral Mucosa and Fractures of the
Mandible.
CLINICAL FEATURES
» Odynophagia with varying degrees of trismus.
» When infection is localized to the sublingual space: structures in the floor
of mouth are swollen and tongue seems to be pushed up and back.
» When infection spreads to submaxillary space: submental & submandibular regions become swollen,
tender, and impart woody-hard feel.
» Tongue is progressively pushed upwards & backwards threatening the airway.
TREATMENT
1) Systemic antibiotics.
2) Incision and drainage of abscess.
a. Intraoral approach—if infection is localized to sublingual space.
b. External approach —if infection involves submaxillary space.
3) Tracheostomy, if airway is endangered.
COMPLICATIONS
1. Spread of infection to parapharyngeal & retropharyngeal spaces and thence to the mediastinum.
2. Airway obstruction due to laryngeal oedema, or swelling and pushing back of the tongue.
3. Septicaemia.
4. Aspiration pneumonia.
----------------------------------------------------------------------------------------------------------------------------------------
2) Thyroglossal fistula [15]
a. Thyroglossal cyst [07, 04]
Ans. Cystic swelling developed in the remnant of thyroglossal tract is called thyroglossal cyst. It is the
commonest retention cyst below the level of the hyoid and is the MC congenital neck mass.
 Sites: �

Clinical Features
Symptoms Signs
Midline swelling seen Cyst can occur anywhere from foramen
in the anterior aspect cecum to the isthmus of thyroid gland
of the neck Swelling moves with deglutition &
protrusion of the tongue
Painless if not infected
'Hood sign': The skin above the fistulous
Infected cyst may opening is pulled upwards by the
rupture & form thyroglossal tract and this gives rise to
discharging puckering of the skin resembling a hood
thyroglossal fistula of a snake
 Investigations:
 Thyroid scan to rule out an ectopic thyroid
 Fistulogram is done if it is associated with fistula, which helps in identifying the extent of the tract
 Treatment is complete surgical excision – Sistrunk’s operation.
 Simple excision of cyst without removal of its tract leads to recurrence.
 Prognosis: The patient should be followed up as papillary carcinoma as well as Hurthle cell adenoma
has been reported to be arising from thyroglossal duct cyst
 Differential Diagnosis: Dermoid cyst, Pyramidal lobe hyperplasia, Thymic cyst & Subhyoid bursitis
----------------------------------------------------------------------------------------------------------------------------------------
3) Laryngocele [2000]
Ans.
Laryngocele refers to an abnormal dilatation of the appendage of the
laryngeal ventricle of Morgagni forming an air-sac lined with
pseudostratified ciliated, columnar epithelium (air-filled dilated saccule)
• It is a unilateral narrow necked, air-containing diverticulum resulting from
herniation of laryngeal mucosa
• It extends between thyroid cartilage and the ventricle.
• Seen in – professional trumpet players, glass blowers and in people with chronic cough
• Bryce sign: In combined laryngocele, neck mass when compressed from outside will cause hissing
sound of air escaping into the larynx
• Treatment is endoscopic or external EXCISION.
----------------------------------------------------------------------------------------------------------------------------------------
4) Pharyngeal pouch [2000]
Ans.
PHARYNGEAL POUCH – aka hypopharyngeal diverticulum or Zenker’s
diverticulum, it is a pulsion diverticulum where pharyngeal mucosa
herniates through the Killian’s dehiscence— a weak area between two
parts of the inferior constrictor.
 Killian’s dehiscence is also called “gateway of tears” as perforation
can occur at this site during oesophagoscopy
AETIOLOGY
» It is formed due to spasm of cricopharyngeal sphincter during the act of deglutition.
» Usually seen after 60 years of age.
PATHOLOGY: Herniation of pouch starts in the midline. It is at first behind the oesophagus and then comes
to lie on its left. Mouth of the sac is wider than the opening of oesophagus and food preferentially enters
the sac.
CLINICAL FEATURES
– appears after a few swallows when the pouch gets filled with food & presses on oesophagus.
is produced on swallowing.
, when patient is recumbent → cough & aspiration
pneumonia.
due to dysphagia.
May be a/w hiatus hernia.
COMPLICATIONS: Carcinoma can develop in long-standing cases of pharyngeal pouch
DIAGNOSIS: Barium swallow will show the sac and its size.
TREATMENT
1) Excision of pouch and cricopharyngeal myotomy: This is done via cervical approach.
2) Dohlman’s procedure – The partition wall between the oesophagus and the pouch is divided by diathermy through an endoscope.
3) Endoscopic laser treatment –by CO2 laser.
1. Define & classify Goitre. Discuss the Etiology, C/F, Dx & Mx of Grave's disease [21, 17, 13]
a. Classify thyroid swellings [17]
b. Thyrotoxicosis – etiopath, symptoms, signs, investigations, Dx, complications & treatment [03]
Ans.
: The term goitre is defined as generalised
enlargement of the thyroid gland.
:�
Thyrotoxicosis
:
Diseases of thyroid : Graves’ disease; Multinodular goitre;
Thyroiditis; Thyroid adenoma
Iodide-induced: Drugs (amiodarone), Iodine
supplementation programme
Extrathyroidal source of thyroid hormone: Factitious
thyrotoxicosis, Struma ovarii
TSH-induced: TSH-secreting pituitary adenoma,
Choriocarcinoma and hydatidiform mole
Follicular carcinoma ± metastases
:�
 Graves’ disease is an autoimmune thyroid disorder
which occurs typically in women aged 30–50 years.
The most common manifestation is thyrotoxicosis +
Diffuse goitre.
 Associations of Grave’s disease:  risk for other
autoimmune diseases like SLE, Pernicious anemia,
Type 1 DM & Addison Disease
 Complications of Grave’s disease:
 Exophthalmos: Due to sympathetic overactivity 
wide, staring gaze and lid lag {typical signs}
 Pretibial myxedema {infiltrative dermopathy}:
presents as scaly thickening & induration of skin
– Life-threatening
complication of thyrotoxicosis. It’s a medical emergency
Causes:
 It is precipitated by infection in a patient with previously
unrecognised or inadequately treated thyrotoxicosis.

 Also seen shortly after thyroidectomy or within a

few days of therapy
Clinical Features: Fever, agitation, delirium,
tachycardia or atrial fibrillation and, in the older
patient, cardiac failure.
Management: Rehydrate + give propranolol, either orally (80 mg 4 times daily) or IV (1–5 mg 4 times daily).
  Sodium ipodate (500 mg per day orally) – This is a radiographic contrast medium that not only inhibits the
release of thyroid hormones but also  the conversion of T4 to T3. Dexamethasone (2 mg 4 times daily) and amiodarone
have similar effects.
 Oral carbimazole 40–60 mg daily – to inhibit the synthesis of new thyroid hormone.

Clinical findings + Laboratory findings will help in Dx

Laboratory findings:  Serum TSH.  Free T4.
Serum TSH is the most useful single screening test for hyperthyroidism, because it is  even at
subclinical stage.
Measurement of radioactive iodine uptake by the thyroid gland to determine the cause.
  uptake in the whole gland  Graves’ disease
  uptake in a solitary nodule  toxic adenoma
  uptake  thyroiditis
�

----------------------------------------------------------------------------------------------------------------------------------------
2. Write about the etiopath, clinical features and Mx of Multi Nodular Goitre [20, 19, 08, 02]
Ans.
Definition: MNG is discordant growth with functionally and
structurally altered thyroid follicles presenting as multiple
nodules in thyroid
Etiology: Fluctuation in TSH level {MCC}; iodine deficiency,
goitrogens, hereditary, Dyshormonogenesis
Clinical Features:
Multiple nodules of different sizes are formed in both lobes –
nontender, moves with deglutition
More common in females; slowly progressive disease with
many years of history
Recent increase in size signifies malignant transformation or
haemorrhage
Positive Kocher's test {compression over trachea}
Complications: Haemorrhage in a nodule, Secondary thyrotoxicosis, Follicular carcinoma of thyroid,
Tracheal obstruction, calcification & cosmetic problem
Investigations:
T3, T4, TSH, free T4, US neck & FNAC.
 X-ray neck – to detect calcification; also reveals compression of trachea
Indirect laryngoscopy to see vocal cords prior to surgery
Routine blood investigations, serum calcium
CT scan/MRI – in cases with retrosternal extension
Treatment: Surgery is preferred – as MNG is irreversible, risk of complications & for cosmetic reasons
Subtotal thyroidectomy – depending on the amount of gland involved
Total thyroidectomy – if entire gland is involved
Postoperative L-thyroxine – to address fluctuation in TSH level
Prevention of MNG –
Correct iodine deficiency by using iodine-rich diet like eggs/seafood/milk or iodized salts and also
avoiding goitrogenic drugs and diet
Start L-thyroxine when patient develops goitre in puberty
----------------------------------------------------------------------------------------------------------------------------------------
3. Classify Carcinoma thyroid and its management [04]
a. Treatment of carcinoma thyroid [12, 08]
Ans.
Classification of Thyroid neoplasms:
Benign neoplasms – Follicular adenoma {Colloid> Fetal> Embryonal> Hurthle cell}
Malignant neoplasm {Dunhill classification}
Differentiated cancers – Papillary carcinoma> Follicular carcinoma> Hurthle cell carcinoma
Undifferentiated cancers – Anaplastic carcinoma
Medullary carcinoma
Malignant lymphoma
Secondaries in thyroid (rare) – from colon, kidney, melanoma, breast
Investigations:
FNAC of thyroid nodule and lymph node – psammoma bodies are found in papillary carcinoma of
thyroid
On table frozen section biopsy is useful in negative FNAC but doubtful cases.
Radioisotope scan shows cold nodule
TSH level in the blood
Plain X-ray neck shows fine calcification
US neck to identify non-palpable nodes in neck and also lymph node.
Serum calcitonin estimation if FNAC confirms medullary carcinoma
Treatment:
Surgery depends on FNAC report as:
 If FNAC report says follicular adenoma  hemithyroidectomy
 If FNAC report says follicular carcinoma of thyroid  Total thyroidectomy + central node
compartment dissection (level VI).
 If FNAC report says papillary carcinoma of thyroid  total thyroidectomy + L thyroxine
 If FNAC report says medullary carcinoma of thyroid  total thyroidectomy + bilateral neck
nodal dissection including central compartment
Post-op L-thyroxine therapy
Radioactive iodine therapy (RAIT) if tumour is multicentric, > 1 cm size, presence of nodes,
extrathyroidal spread, high-risk group
--------- -------------------------------------------------------------------------------------------------------------------------------
4. Discuss the DD and Mx-of Nodule in the Thyroid [03]
 a. Solitary Nodular goiter – C/F, Dx & Complications [19, 18]
b. Solitary toxic nodule [16]
c. Thyroid nodule [05]
Ans.
: Solitary Nodular goiter refers to a single palpable nodule in thyroid on clinical & radiological
{USG neck} examination, in an otherwise normal gland. Rest of the gland is impalpable.
:
Follicular adenomas {Colloid> Fetal> Embryonal> Hurthle cell}
Carcinomas {Papillary> Follicular> Medullary}
Thyroid cysts
Localised thyroiditis
:
Based on function – 2 types – Toxic solitary nodule & Nontoxic solitary nodule
Based on radioisotope study – 3 types – Hot {overactive}, warm {normal functioning} & cold {underactive}
:
Single nodule palpable in one lobe – smooth, firm
Commonest site of a nodule is at the junction of isthmus with one of the lateral lobes
Tracheal deviation towards opposite side – confirmed by trail sign, three-finger test, auscultation
and X-ray neck.
Lahey's test does not show any other nodules in posterior part of the gland
Features of malignant changes: Rapid enlargement of nodule, fixity of nodule, nodule in extremes
of age, Hoarseness of voice/dysphagia/stridor/dyspnoea, palpable neck nodes etc.
:
USG neck – TIRADS-Thyroid Imaging Reporting & Data system – 1 {benign} to 5 {highly suspicious of malignancy}
FNAC
Radioisotope study – to know functioning status – warm or hot or cold?
T3, T4, TSH
Power Doppler – to know the vascularity of the gland {malignant nodules are highly vascular}
Serum calcitonin estimation if FNAC confirms medullary carcinoma.
X-ray neck to see tracheal deviation.
:
For benign solitary nodule – regular follow-up
For benign solitary toxic nodule – antithyroid drugs;
occasionally surgery is done – hemithyroidectomy.
For malignant nodule – surgery depends on FNAC report as:
 If FNAC report says follicular adenoma  hemithyroidectomy
 If FNAC report says papillary carcinoma of thyroid  total thyroidectomy + L thyroxine
 If FNAC report says medullary carcinoma of thyroid  total thyroidectomy + bilateral neck
nodal dissection including central compartment
----------------------------------------------------------------------------------------------------------------------------------------

1) Complications of Thyroidectomy [21]

Ans.
----------------------------------------------------------------------------------------------------------------------------------------
2) Exophthalmos [15, 05]
Ans.
It is proptosis of the eye, caused by infiltration of the retrobulbar tissues with fat, fluid and round
cells, with lid spasm of upper eyelid
Exophthalmos is visible sclera first lower part and later eventually upper part of sclera will be
visible.
Proptosis can be measured by exophthalmometer
:
Endocrinal: Thyrotoxicosis {MC}; Cushing's syndrome, acromegaly-rare
Inflammatory: Orbital cellulitis, frontal sinusitis
Other eye causes: Severe myopia; Severe glaucoma – Buphthalmos
Vascular causes: Cavernous sinus thrombosis/A-V fistula; Ophthalmic artery aneurysm
Congenital deformities of skull: Craniostenosis, oxycephaly, hypertelorism
Primary tumours: Periorbital meningioma; Optic nerve glioma; Orbital haemangioma;
Lymphoma; Osteoma
Secondary tumours: Antral carcinoma, neuroblastoma
:
 Moebius sign – early sign of ophthalmoplegia
 Severe Exophthalmos is a/w chemosis, conjunctival injection & corneal ulceration
: identify & treat the cause – Example:
Antithyroid drugs + steroids
Antibiotic drops; 1 % methylcellulose eye drops to prevent corneal ulceration
Lateral tarsorrhaphy; Orbital decompression by surgical removal of lateral wall or roof of orbit
Dark spectacles, protective eye patches
----------------------------------------------------------------------------------------------------------------------------------------
3) Hashimoto's thyroiditis [14, 09, 2000]
Ans. “Autoimmune thyroid disease – aka diffuse non-goitrous thyroiditis”. MC cause of hypothyroidism
: 45-65 yrs
: F>M
: Breakdown of self-tolerance to thyroid
autoantigens → autoantibodies form against
thyroglobulin & TPO.
 Initially they present with toxic features, but later, they manifest with features
of hypothyroidism + goitre
:
FNAC
TFT: Raised TSH; Low free T3, T4;
Antibodies: Anti thyroglobulin & anti TPO antibodies;
Ultrasound; FNAC; Biopsy → shows Hürthle cells & lymphocytes
: other autoimmune diseases – SLE, Sjogren syndrome, Type 1 DM
papillary carcinoma of thyroid; Extranodal marginal zone B-cell lymphoma

• L-thyroxine therapy + Steroid therapy

• If goitre is large and causing discomfort, then subtotal thyroidectomy is done
----------------------------------------------------------------------------------------------------------------------------------------
4) Thyroid Function Tests [07]
Ans.

----------------------------------------------------------------------------------------------------------------------------------------
5) Lateral aberrant thyroid [02]
Ans.
Lateral aberrant thyroid is a mass of tissue having the structure of a thyroid gland, but situated at
some definite distance from the normal thyroid, with which it has no connection, or more strictly,
lateral to the jugular vein.
Etiology: it is due to metastatic deposit from papillary carcinoma of thyroid.
confirms the diagnosis and is treated like metastatic papillary carcinoma thyroid.
1. Multiple Endocrine Neoplasia (MEN) [21, 20]
Ans.
MEN/MEA {Multiple Endocrine Neoplasia/ Adenomatosis} is an endocrine syndrome complex usually
inherited as autosomal dominant, but occasionally it can be sporadic.
MEN type Gene involved Major tumours Management
 Serum prolactin, MRI head  Trans-
MEN 1 3 P sphenoidal pituitary surgery + radiotherapy
MEN 1 ituitary adenoma
{Menin}   Serum calcium, PTH, Tech99 labelled
{Wermer  arathyroid hyperplasia
gene sestamibi isotope scan, imaging of neck 
Syndrome}  ancreatic tumours {esp.
mutation of islets} Total parathyroidectomy
 MRI and Endosonography for pancreas

 arathyroid
MEN 2A
hyperplasia
{Sipple’s
 edullary thyroid
Syndrome}  Serum calcium, PTH, Tech99 labelled
carcinoma
sestamibi isotope scan, imaging of neck
RET  heochromocytoma
 Relevant Biochemical investigations
mutation in  Total parathyroidectomy, thyroidectomy &
MEN 2B chromosome 10  heochromocytoma
adrenalectomy is the treatment
{Multiple  edullary thyroid
mucosal carcinoma
neuroma  ucosal neuromas,
syndrome} with marfanoid face
& megacolon
----------------------------------------------------------------------------------------------------------------------------------------
2. Hypercalcaemic crisis [20]
Ans.
:
Sudden increase in PTH level due to rupture of parathyroid cyst or bleeding in the parathyroid
tumour.
Severe dehydration may precipitate the crisis.
Secondaries in bone (primary may be from breast).
: abdominal pain, vomiting, dehydration, oliguria, muscular weakness and death.
: Serum Ca+2 is very high > 12 mg/dl (Normal Ca+2 levels: 8.5-10.5 mg/dl).

Forced diuresis using 3-5 litres of saline with

frusemide.
Rehydration using normal saline 300 mL/hour.
Steroids - to inhibits effects of vitamin D – Dose is 400
mg/day IV for 5 days.
Clodronate sodium, Pamidronate (90 mg IV slowly in
4 hours, is a bisphosphonate) – Inhibits mobilization
of the calcium from the bone).
 Drugs to reduce Ca+2 levels – mithramycin, calcitonin, cinacalcet {Ca+2 receptor agonist},
prednisolone, bisphosphonates & Gallium nitrate {inhibits osteoclast resorption of calcium} at a
dose of 200 mg/m2/day for 5 days. Condition has high mortality rate.
: Patient develops hyperchloremic metabolic acidosis;
---------------------------------------------------------------------------------------------------------------------------------------
3. Parathyroid adenoma [15, 97]
a. Recurrent Hyperparathyroidism [20]
b. Parathormone [03]
c. Primary Hyperparathyroidism [02, 87]
Ans.
Hyperfunctioning of parathyroid gland with elevated PTH levels.
Types:
1) Primary Hyperparathyroidism
2) Secondary Hyperparathyroidism
: “An autonomous overproduction of PTH is seen.” MC cause of
asymptomatic hypercalcemia.
 : Adenoma (MC); Primary hyperplasia; Carcinoma
 : Elderly Female
It can be Sporadic (MC) or Familial
Genetic alterations with sporadic adenomas:
1) Cyclin D1 gene inversions leading to overexpression of cyclin D1
2) Mutations involving MEN1 tumor suppressor gene
Familial parathyroid adenomas; They are seen with MEN-1 & MEN-2A, caused by germline
mutations of MEN1 & RET.
Clinical Presentations: Asymptomatic or can exhibit the following symptoms {"Bones, stones,
abdominal groans and psychiatric moans"}:
 Bone: Osteoporosis & osteitis fibrosa cystica leading to fractures.
 GIT: Constipation, nausea, peptic ulcers, & pancreatitis
 Renal: Nephrolithiasis & chronic renal insufficiency
 CNS: Depression, lethargy, & seizures
 Neuromuscular: Weakness & fatigue
 Cardiac: Aortic or mitral valve calcifications
Inv.: Elevated PTH levels, Hypercalcemia, hypophosphatemia, increased urinary excretion of both
calcium & phosphate.
: “Compensatory overactivity of the parathyroid glands due to
chronic hypocalcemia.”
 Causes: Renal failure (MC), inadequate intake of calcium, Vit. D deficiency, & steatorrhea.
 Clinical Presentations:
1) Features of chronic renal failure
2) Milder skeletal abnormalities
3) Ischemic damage to tissues (calciphylaxis)
Treat the cause {Ex: surgical excision of the hormone secreting tissue}.
 Orthopedic treatment – directed towards adequate protection of the softened bones from all
deforming stress and strain.
 Urology treatment – directed towards the removal of calculi and maintenance of renal functions.
----------------------------------------------------------------------------------------------------------------------------------------
4. Phaeochromocytoma [02, 74]  {refer pg. no. 101 in Medicine-Paper I}
a. Mx of Phaeochromocytoma [21]
----------------------------------------------------------------------------------------------------------------------------------------

1) Symptoms and sings of Cushing syndrome [14]  {refer pg. no. 91 in Medicine-Paper I}
----------------------------------------------------------------------------------------------------------------------------------------
2) Von Recklinghausen's disease [13]
Ans.
Aka Type 1 Generalised neurofibromatosis – it is an inherited autosomal dominant disease wherein
there will be multiple neurofibromas in the body due to a defect in chromosome 17
 It may be cranial, spinal or peripheral.
 It is associated with pigmented spots (coffee coloured) in the skin, commonly seen on the back,
abdomen, thigh (cate-au-lait spots) – signifies common neuroectodermal origin of nerve sheath
cells and melanocytes
 Also seen in MEN-2B
 Treatment: Excision under general or regional anaesthesia
1. Tetanus – etiopath, C/F, Mx & DDx [05, 01, 91]
Ans.
Tetanus is an infectious disease caused by clostridium tetani

 Virulence Factors – 2 exotoxins: tetanolysin and

tetanospasmin.
 Mode of Transmission:
a. Injury (superficial abrasions, punctured wounds, RTA).
b. Surgery done without proper asepsis
c. Neonates: Following abortion/ delivery, due to unhygienic
practices
Clinical Manifestations
 Muscles of the face and jaw are affected first (shorter distances
for the toxin to reach the presynaptic terminals)
 1st Symptom: Increase in the masseter tone {trismus or lock jaw}
 In neonates, difficulty in feeding is the usual presentation.
 As the disease progress, generalized painful muscle spasm 
leads to descending spastic paralysis.
 Hands, feet are spared & Deep tendon reflexes are exaggerated.
Complications:
a. Risus sardonicus: sustained spasm of the facial muscles that
appears to produce grinning.
b. Opisthotonos position: occurs due to generalized spastic
contraction of the extensor muscles.
c. Respiratory muscles spasm → May cause airway obstruction
DDx: hypocalcaemia, meningitis, seizure, strycnine poisoning,
dystonia reaction to phenothiazines, odontogenic abscess etc.
Mx �
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1) Carbuncle [21, 17, 10, 07, 05, 03]

Ans.
Carbuncle (meaning “charcoal”): It is an infective gangrene of
skin and subcutaneous tissue.
Causative agent: Staphylococcus aureus
Predisposing factors: elderly males; diabetics
Clinical presentation:
Carbuncle is cluster of furuncles connected
subcutaneously, causing deeper suppuration and scarring.
Common site of occurrence is nape of the neck and back {skin in this area is thick}
Investigations: Urine sugar and urine ketone bodies; Blood sugar; Discharge
for C/S.
Treatment:
Control of diabetes
Antibiotics like penicillins, cephalosporins – depending on C/S.
Drainage is done by a cruciate incision + Debridement of all dead tissues
 Excision  after wound granulates well  skin grafting
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2) Abscess [21, 04]
a. Hilton's method of opening on abscess [13]
b. Acute abscess [07, 06]
Ans.
Definition: Abscess is a localised collection of pus in a cavity lined by
granulation tissue, covered by pyogenic membrane
 Pus contains dead WBC's, multiplying bacteria, toxins & necrotic material
 Protein exudation causes fibrin deposition and formation of pyogenic
membrane
Causative Organism: Staphylococcus aureus; Streptococcus pyogenes; Gram-negative bacteria (E. coli,
Pseudomonas, Klebsiella); Anaerobes.
Mode of infection: Direct; Haematogenous; Lymphatics; extension from adjacent tissues
Clinical features:
 Fever often with chills and rigors.
 Rubor (redness); dolor (pain); calor(warmness); tumour (swelling) and functio laesa (loss of
localised and adjacent tissue/joint function) are quite obvious
 Localised swelling is smooth, soft and fluctuant with visible (pointing) pus.
 Throbbing pain and pointing tenderness and Brawny induration around.
 Visible (pointing) pus, tenderness, fluctuation are the
features of formed abscess.
Investigations:
 CBP: WBC;
 Urine sugar and blood sugar – to r/o diabetes
 Chest X-ray is done in case of lung abscess
 USG of the part
 Investigations, relevant to specific types: LFTs, CSF, blood
culture etc.
DDx: Aneurysm, Soft tissue tumours, Haematoma. & Cold
abscess
Treatment of Abscess: treat the cause & drain the abscess
Hilton's method of draining an abscess:
Start the patient on broad-spectrum antibiotics  Under
anaesthesia, after cleaning and draping, aspirate the abscess & confirm the presence of pus 
Incise the skin in the line parallel to the neurovascular bundle in the most dependent position.
Open the pyogenic membrane using Sinus forceps & break all loculi are broken up.
 Abscess cavity is cleared of pus and washed with saline. A drain (either gauze drain or corrugated
rubber drain) is placed. Wound is not closed. Wound is allowed to granulate and heal.
Pus is sent for culture and sensitivity. Biopsy should be done in suspected TB or malignancy.
Sometimes secondary suturing or skin grafting is required. Antibiotics are continued.
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3) Cellulitis [20, 06]
Ans.
: It is spreading infective inflammation of subcutaneous tissue and fascial planes
: a small scratch or wound or incision or insect/snake/scorpion bite
:
Swelling is diffuse and spreading in nature + Fever, toxicity
(tachycardia, hypotension)
Pain & tenderness, red, shiny area with stretched warm skin
Tender regional lymph nodes
No edge; no pus; no fluctuation; no limit.
: DVT of lower limb

 CBP: WBC, platelet count

 LFTs, blood urea and serum creatinine in severe cases.
 Blood sugar estimation, urine test for ketone bodies, glycosylated haemoglobin estimation.
 Venous Doppler and ultrasound of soft tissues of the limb – to /.

Elevation of limb & bandaging – to reduce oedema & to increase the circulation.
Antibiotics – penicillins, cephalosporins.
Glycerine Dressing – as it reduces the oedema because of its hygroscopic action.
Diabetes to be treated with insulin.
Often patient may be in septicaemia & should be managed as per the protocol
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4) Antibioma [18, 14, 10]
Ans.
If intramammary mastitis is not drained but only treated by antibiotics, pus localises and becomes
sterile with a thick fibrous tissue cover and it is called as antibioma.
Clinical Features:
 Previous history of mastitis treated with antibiotics.
 Swelling – painless, smooth, non-tender, hard, fixed to breast tissue without involving the
pectorals and chest wall.
DDx: Carcinoma breast (Scirrhous carcinoma breast).
Investigations: FNAC; mammography; US breast.
Treatment: 1st Excision (Submammary incision)  Later, antibiotics. It should be sent for histology.
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5) Hidradenitis Suppurativa [08]
Ans. : It is a chronic scarring inflammatory acne like
disease of the skin bearing apocrine sweat glands {which open into
hair follicles}. It is aka ‘acne inversa’
: Smoking, female, obesity, poor hygiene, PCOD, DM,
steroid therapy, PASH syndrome etc.
 :
MC site is axilla - Multiple discharging sinuses, with tender nodules in the
skin
Induration due to fibrosis.
: Tuberculous sinus; Malignancy; Lymph node mass
:
Discharge study-culture/sensitivity and AFB.;
Biopsy to rule out tuberculosis or malignancy
:
Topical clindamycin 1%; topical resorcinol 15% cream.
Oral antibiotics like clindamycin, erythromycin, doxycycline-needs longer course.
Antiandrogen therapy in females
Infliximab, retinoids – used in severe cases.
Wide excision (radical excision) of the involved area with skin grafting.
Alternative: Ablative laser (CO2 or erbium YAG) therapy
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6) Gangrene [06]
a. Diabetic Gangrene [19, 13, 07]
b. Fournier's gangrene [17, 07]
c. Gas gangrene [16, 14, 09, 04]
d. Direct and indirect traumatic gangrene [16, 14]
Ans.

:
Diabetic microangiopathy causes blockade of microcirculation leading to hypoxia
Due to sensory neuropathy, minor injuries are not noticed and so infection occurs {High glucose
level in tissues is a good culture media for bacteria} more prone for trauma & infection
Also, Diabetic atherosclerosis itself reduces the blood supply and causes gangrene.
:
Pain in the foot; Ulceration; Absence of sensation
Abscess formation; Change in temperature and colour
Absence of pulsations in the foot & Loss of joint movements
Patient may succumb to ketoacidosis, septicaemia or myocardial infarction.
:
Blood sugar, urine ketone bodies.
Glycosylated haemoglobin estimation
Blood urea and serum creatinine
X-ray of part to look for osteomyelitis.
Pus for culture and sensitivity
Doppler study of lower limb to assess arterial patency
Ultrasound of abdomen to see the status of abdominal aorta
: Foot can be saved only if there is good blood supply
Control diabetes via insulin; Diet control, control of obesity
Antibiotics – based on pus C/S.
Regular dressing
Drugs: Vasodilators, low dose aspirin.
 Care of feet in diabetic – Keep feet clean & Dry; Wear rubber footwears; Avoid injury
Surgical debridement of wound; Amputations of the gangrenous area

– It is also called as idiopathic gangrene of the scrotum

It is a vascular gangrene of infective origin, caused by haemolytic streptococci, microaerophilic
streptococci, staphylococci, E. coli, Cl. Welchii, Bacteroides fragilis
: diabetics, old age, malnourished, immunosuppressed individuals
:
 Sudden pain in the scrotum, fever, severe toxicity
 Extensive skin sloughing occurs leaving normal testis expose
 Very fast spreading cellulitis of scrotal skin, extending to the groin and often to anterior
abdominal wall  renal failure and other complications  death
:
IV fluids and catheterisation-for maintenance of urine output
Antibiotics, blood transfusion & Nutritional support (TPN, enteral).
Liberal excision of all slough
Once patient recovers and wound granulates well, skin grafting is done
Testis can be placed in the pouch in medial aspect of the thigh  Orchidectomy is not necessary as
testis is normal and viable

Features Dry Gangrene {indirect traumatic} Wet Gangrene

Occurs in moist tissues or organs
Common site Limbs (MC lower limb)
(e.g., GIT)
Gangrene due to atherosclerotic
Ex. Diabetic foot, Bed sores etc
narrowing of blood vessel of lower limb
Etiological factors
Arterial obstruction (due to Venous obstruction (e.g.,
atherosclerosis, thromboangiitis strangulated hernia,
Cause of ischemia
obliterans (Buerger’s disease), Raynaud’s intussusception or volvulus)
disease, trauma, ergot poisoning etc.)
Rate of obstruction Slow Abrupt
Gross features
Appearance Shriveled dry (mummification) and black Swollen, soft, putrid and dark
Line of demarcation Clear cut Not Clear cut
The necrosis (predominantly coagulative
type) shows smudging of soft tissue and
Microscopy overlying skin. The line of demarcation Liquefactive type of necrosis
consists of granulation tissue with
inflammatory cells
Spread Slow Rapid
Poor due to severe
Prognosis Fair (due to little septicaemia)
septicaemia
 : is defined as a rapidly spreading,
edematous myonecrosis a/w crushed wounds contaminated with pathogenic clostridia.
Gas gangrene is always polymicrobial & is caused by C. perfringens (most
common, 60% of the total cases) and C. novyi and C. septicum (20-40%)
1. Gas bubbles (crepitus) in the muscle planes
2. Brawny edema and induration
3. Shock and organ failure develop later  jaundice
:
» X-ray shows gas in muscle plane or under the skin
» Gram's stain shows Gram-positive bacilli; Robertson's cooked meat media is used for culture
» Liver function tests, blood urea, serum creatinine, total count etc.
» CT scan of the part

a. Early surgical debridement of devitalized tissues.

b. Abx: Penicillin + Clindamycin for 10-14 days.
c. Hyperbaric oxygen: to kill the obligate anaerobic clostridia
d. Passive immunization with anti-α-toxin antiserum.
e. Fresh blood transfusion – for hypotension
f. In severe cases amputation has to be done as a life-saving procedure
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7) Hospital infection [05]  refer pg. no. 92 in Medicine – Paper 2
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1) Methicillin Resistant Staphylococcus Aureus [19]

Ans.
Methicillin resistance in S. aureus is mediated by a chromosomally coded gene called mec A gene,
which alters penicillin-binding protein (PBP) present on S. aureus cell membrane to PBP-2a.
 PBP is an essential protein needed for cell wall synthesis of bacteria. β lactam drugs inhibit PBP.
 The altered PBP2a of MRSA strains has less affinity for β-lactam antibiotics; hence, MRSA strains
are resistant to all β-lactam antibiotics
 Types of MRSA: �
 Detection of MRSA:
 Antimicrobial susceptibility test: Disk diffusion test
can be done by using cefoxitin disc
 PCR: to detect mec A gene
 Latex agglutination test: to detect PBP-2a.
 Treatment:
 DOC for MRSA: Vancomycin
 For nasal carriers of MRSA, mupirocin ointment is used
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2) Necrotising Fasciitis [10]
Ans.
Necrotizing Fasciitis – aka Hemolytic streptococcal gangrene
 Source of the infection: 2 – Traumatized skin & GIT breach (due to abdominal surgery releasing the bowel
flora)
  GAS invade the muscles → produce SPE – B  severe pain, fever, chills, Skin develops mottled
erythema and anesthetized (due to infarction of the cutaneous nerves) with extensive necrosis
of subcutaneous tissue, fascia and muscle (Hence, GAS is also called as flesh-eating bacteria)
 Treatment: Early drainage of inflammatory fluid & Debridement of necrotic area; DOC – Pen G +
Clindamycin
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3) Actinomycosis [08]
Ans.
It is chronic suppurative disease with systemic illness.
Actinomycetes israelii (G+ve, filamentous anaerobic bacteria)
 Break in mucocutaneous continuity, diminished immunity favors the organism to invade,
proliferate and disseminate
M>F
Endogenous
Suppurative & granulomatous inflammation with the formation of abscesses sulphur
granules (Splendore –Hoeppli phenomenon).
: Biopsy, culture & immunofluorescence staining. They stain positively with Gomori’s
methenamine silver (GMS) stain
Risk Factors Sites involved
Swelling develops in the lower jaw (lumpy
jaw) with abscess & sinus tract
Dental caries, periodontal disease or
1 Cervicofacial formation. May extend to involve
trauma following extraction of tooth
mandible, orbit, cranial bones or CNS.
Sinus discharges yellow sulfur granules
Aspiration of organism from the oral
Lungs are involved commonly, may
2 Thoracic cavity or extension of infection from
extend to pleura & chest wall
abdominal or hepatic lesions
Swallowing of organism from oral
3 Abdominal cavity or as an extension from Appendix, cecum and liver
thoracic cavity
4 Pelvic Usage of IUCD
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4) Collar stud abscess [07, 95]
Ans.
 A collar stud abscess is an acute suppurative infection
presenting as a stud-like blister.
 Investigations: X-ray of the part is required often to rule out
osteomyelitis of terminal phalanx; Pus for culture and sensitivity to be sent
 Treatment: Antibiotics and analgesics; Incision & drainage of the abscess
1) Implantation dermoid [21, 03]
Ans:
It is an acquired cystic lesion lined by epithelium
: Minor pricks or trauma  epidermis gets buried into the
deeper subcutaneous tissue reaction & cyst formation (trauma is forgotten often)
:
 Swelling is painless, observed after minor trauma & is slowly progressing
 Sites: fingers (common in tailors, gardeners), toes and feet.
 It is smooth, soft, mobile, tensely cystic, non-transilluminating and is often adherent to skin.
 It contains only squamous epithelium, without hair follicle/ sweat or sebaceous glands.
are infection, rupture and pressure effect over digital nerves.
: Lipoma, bursa.
: Excision-under local anaesthesia.
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2) Sebaceous cyst [16, 13, 04]
a. Cock's peculiar tumor [16, 02]
b. Complications of sebaceous cyst [09]
Ans:
It is a retention cyst.
It is due to blockage of the duct of sebaceous
gland, causing a cystic swelling.

Swelling is painless, smooth, soft, freely mobile, adherent to skin especially over the summit,
fluctuant (positive Paget's test), non-transilluminating with punctum over the summit.
It moulds on finger indentation; Unpleasant odour of sebum content; Hair loss over the surface
Sebaceous cyst contains fat and epithelium. It has putty like consistency, with a parasite in the wall
of the sebaceous cyst-Demodex folliculorum
Sites: It is common in face, scalp, scrotum. It is not seen in palms and soles as there are no
sebaceous glands
(Fordyce's disease is heterotopic sebaceous glands in mucosa of the lip and oral cavity).
: Infection and abscess formation.
Surface may get ulcerated  painful, fungating mass with discharge
called as-Cock's peculiar tumour-often resembles epithelioma.
 It is a misnomer as it is not a tumour.
 It is a chronic granuloma on an ulcerated surface of a sebaceous cyst.
Sebaceous horn results from hardening of slowly discharged sebum through the punctum

Excision including skin adjacent to punctum using elliptical incision-dissection method.

Incision and avulsion of cyst wall.
If abscess is formed, then drainage initially and later excision is done.
If capsule is not removed properly the cyst will recur.
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3) Desmoid tumor [15, 11, 08]
Ans.
: It is a tumour arising from the musculoaponeurotic layer of abdomen, below the level
of the umbilicus
It is unencapsulated, hard, fibroma, presently classified under aggressive fibromatosis
: female; OCPs; after deliveries; old abdominal operation scars; Gardner's syndrome.
: It is a slow growing tumour involving muscle and soft tissue of the abdominal
wall, locally spreading, often undergoes myxomatous changes {unlike fibromas, it never turns into
sarcoma}
:
 Look for association with Gardner's syndrome - Barium enema, X-ray, US abdomen, MRI
 Biopsy is done to confirm the diagnosis.
 Wide excision of the tumour with a margin of 2.5 cm + mesh to the abdominal defect
 It is moderately radiosensitive; Chemotherapeutic agents like doxorubicin, actinomycin D,
dacarbazine, carboplatin can also be used
 Recurrence can occur
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4) Epidermoid cyst [08]
Ans.
Epidermoid (Epidermal) Cyst
: It is a benign cyst often also called as epidermal/keratin/infundibular/follicular
infundibular/sebaceous cyst.
:
 Epidermal cells from the infundibulum of the hair follicle proliferates within the dermal space. It is
lined by stratified squamous epithelium
 Precipitating factors: Exposure to UV light and HPV infection.
 It can be autosomal dominant hereditary or acquired
:
In neonates & younger age – Tiny superficial cysts called as Milia are common
Trichilemmal or pilar cysts – mostly seen in scalp of middle-aged females
Epidermal cyst contains cheese like material often with typical foul smell.
Sites: It is common in face, trunk, neck, extremities and scalp.
: Gardner's syndrome, Basal cell naevus syndrome.
Management:
 Inflamed uninfected epidermoid cyst – resolve spontaneously; but tend to recur
 Injection of Kenalog into inflamed lesion – can hasten the resolution
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5) Lipoma [05]
Ans:
: It is a benign neoplasm arising from yellow fat.
:
A lipoma is composed of mature adipocytes and uniform nuclei that are identical to those seen in
normal adult fat.
Lipoma can be superficial or deep; single or multiple
It is the most common benign tumour; It is called as universal tumour (ubiquitous tumour) as it
can occur anywhere in the body except brain. It can be localised (encapsulated) or diffuse
(nonencapsulated).
 – difficult to remove surgically. Recurrence is high after incomplete removal.
Adiposa dolorosa (Dercum's disease) is a multiple lipomatosis mainly seen in females; there is
tender fat deposition especially in the trunk and girdles; it is common in epileptic & psychiatric patients.

Localised swelling, which is lobular (surface), non-tender, non-transilluminant, Mobile, with edges
slipping between the palpating fingers (slip sign); Skin is free.
Lipomas may be pedunculated at times.
Pain in lipoma may be due to neural element or compression to nerves or adjacent structures.
Sites: Trunk {MC}; nape of neck and limbs.
: Ultrasound or CT or MR imaging is done in deep or large or intracavitary lipomas; FNAC
or incision biopsy is needed to confirm it as benign.
:
 Myxomatous changes – occurs in retroperitoneal lipoma.
 Saponification; Calcification.
 Submucosal lipoma can cause intussusception and intestinal obstruction.
 Recurrence
: Excision – small lipoma is excised under local anaesthesia and larger one under general
anaesthesia.
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6) Neurofibroma [04]
Ans. Definition: It is a benign tumour arising from connective tissue of the nerve containing
ectodermal, neural and mesodermal connective tissue components
Sites: Cranial; Spinal; Peripheral
 Neurofibroma is the MC intradural extramedullary spinal tumour
Clinical Features:
Mild pain or Painless swelling with tingling, numbness and paraesthesia along the distribution of
cutaneous nerve.
Swelling moves perpendicular to the direction of the nerve but not along the longitudinal direction
{neurilemmoma has got free mobility in all directions}
Swelling has smooth surface & firm consistency
Cafe-au-lait spots – signify common neuroectodermal origin of nerve sheath and melanocytes
Plexiform neurofibromatosis commonly involves trigeminal cranial nerve
Complications:
Cystic degeneration; Haemorrhage into the tissues.
Spinal and cranial neurofibromas  neurological deficits.
Erosion into deeper planes, bone, orbit;
Muscle atrophy.
Intestinal neurofibroma may precipitate intussusception
Spinal dumbbell tumour can cause compression of spinal cord and paralysis of the limb.
Sarcomatous changes  rapid enlargement, warmness, more vascularity with dilated veins
Investigations: FNAC; MRI
Treatment:
Indications for Surgery – pain & pressure symptoms, cosmetic reasons, malignant transformation
Excision under general or regional anaesthesia
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1. Glomus tumour [06]
Ans.
Aka glomangioma/angioneuroma – It arises from the cutaneous glomus composed of a tortuous
arteriole which communicates directly into the venule and these vessels being
surrounded by network of small nerves making this lesion very painful
:
 Severe burning sensation and pain {MC site is nail-bed} out of proportionate to the
size of purple red swelling {Dilated vessels compress over nerves}
 Pain is aggravated by cold stimulus
 Pain disappears on increasing the pressure in the arm above systolic
: Pyogenic granuloma; Subungual melanoma
: Excision cures the condition
1) Discuss fluid and electrolyte balance and management of Hypokalemia [19, 04]
a. Role of water electrolyte balance in surgical practice [17, 15]
b. Hypokalaemia [16, 11]
c. Potassium Depletion [05]
Ans.
Fluid and electrolyte balance: {Talk about RAAS from physio}
Normal values: �
Hypokalaemia is defined as existing when serum K+ falls below 3.5 mmol/L.
Causes of HYPOkalaemia
- Dietary deficiency
1. Reduced intake
- Potassium-free intravenous fluids
 Alkalosis
2. Redistribution  Insulin & Catecholamines
into cells (flux of  β- agonists
K+ into cells)
 Hypokalaemic periodic paralysis
↑ Activation of mineralocorticoid receptor – seen in - Conn’s syndrome
Cushing’s syndrome, Glucocorticoid excess & Carbenoxolone/liquorice
– iddle’s syndrome, itelman’s syndrome, artter’s
3. Increased urinary syndrome
excretion Renal tubular acidosis
Acetazolamide
Diuresis: Loop diuretics, Thiazides, Recovery from renal obstruction etc.
 Upper GIT – a/w metabolic alkalosis – Vomiting, Nasogastric aspiration
4. Increased GI loss  Lower GIT – a/w metabolic acidosis – Diarrhoea, Laxative abuse, Villous
adenoma, Bowel obstruction/fistula & Ureterosigmoidostomy
Clinical Features of HYPOkalaemia
 Muscular weakness and tiredness.
 Ventricular ectopic beats (arrhythmias)
 Electrocardiogram (ECG) changes: �
 Functional bowel obstruction – occur due to paralytic ileus.
 Renal tubular damage – in chronic cases
Management
First determine the cause & then correct Hypokalaemia with Potassium chloride tablets or i.v.
Potassium chloride
If Hypokalemia is a/w Acidosis – then use Potassium bicarbonate
The rate of administration depends on the severity of hypokalaemia
Correct hypomagnesemia {since low cell magnesium can promote tubular potassium secretion into urine}
, such as amiloride can be used especially when renal loss of potassium
is the underlying cause.
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2) Describe Parenteral Fluid Therapy [08]
a. Total Parenteral Nutrition (TPN) [21, 12]
Ans.
: it refers to nutritional requirements given through IV route.
 It can be through a central catheter through the subclavian/internal jugular vein where the tip of
venous catheter is at distal part of superior vena cava.
 It can also be a peripheral (Peripheral parenteral nutrition/ PPN) through a peripherally inserted
central venous catheter (PICC) or through a formal peripheral venous line.

Failure or contraindication for any enteral nutrition for 7-10 days

High output abdominal fistulas, duodenal, biliary, pancreatic fistulas
Major abdominal surgeries of liver, pancreas, biliary, colonic
Septicaemia; multiple traumas, short bowel syndrome
Severe pancreatitis, bowel ischaemia, peritonitis, ileus
Massive GI bleeding, unstable haemodynamically
High risk of aspiration Hyperemesis gravidarum
Multiorgan failure, head injury, severe burns
: Using a needle and guide wire a Subclavian vein catheter is passed just below the
clavicle and fixed securely to the skin.
 TPN is given through central vein and not through a peripheral vein.

to protein synthesis, to protein breakdown, to prevent weight loss.

To support ongoing metabolism.
To improve immune function, cardiac and respiratory function.
To maintain glycogen reserve in cardiac and respiratory muscles.
To maintain acid, base and electrolyte metabolism.
Underlying disease, its severity, therapies for the disease, GI function should be assessed.

 Carbohydrates – Dextrose. Rate of administration of dextrose is 5 mg/kg/min.

 Fat: Fat gives high calorie. It is given as emulsion containing long chain triglycerides.
 Amino acids: They are source of proteins. In PN 20% of energy comes from amino acids; rest from
dextrose and fat.
 Vitamins, electrolytes, trace elements and minerals: Electrolytes like sodium, potassium,
magnesium, phosphate, calcium; fat-soluble vitamins like A, D, E, K; water-soluble vitamins; trace
elements like chromium, copper, iodine, iron, manganese, selenium, zinc are all used in PN.

 Technical: Air embolism; Pneumothorax; Bleeding; Catheter displacement, sepsis, blockage;

Infection, thrombosis.
 Biochemical
 Electrolyte imbalance: Hyponatraemia, hypokalaemia, hypophosphatemia.
 Hyperosmolarity; Hyperglycaemia-common.
 Dehydration; Azotaemia
 Altered immunological and reticuloendothelial function.
 Others: Dermatitis; Anaemia & capillary permeability; Cholestatic jaundice (It is common); Severe
hepatic steatosis; Metabolic acidosis; Candida infection (candidiasis), staphylococcal infection
 : Cardiac failure; Blood dyscrasias; Altered fat metabolism.
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1. Metabolic Acidosis [21]

Ans.

Identify & treat the cause first.

Shock should be treated with aggressive fluid therapy and adequate oxygenation.
Vasoactive agents (dopamine, dobutamine) should be added only after volume replacement as
they can worsen acidosis.
Routine IV sodium bicarbonate for metabolic acidosis is not recommended.
Sodium bicarbonate is indicated in the following situations:
- When pH is below 7.15
- In cases of Salicylate poisoning
- Inborn errors of metabolism
Amount of Sodium bicarbonate is calculated using the formula: HCO3– deficit (mEq) = 0.5 × body
weight (Kg) × (desired—actual serum HCO3–)
Potassium supplementation to prevent hypokalemia in cases such as DM
Calcium gluconate therapy if Hypocalcemia is precipitated by correction of metabolic acidosis
In severe cases of metabolic and respiratory acidosis, THAM (Tris-hydroxymethylaminomethane) is
more effective buffer used at a dose (mL) = weight (kg) × base deficit, over 3 × 6 h because it
neutralizes acid without releasing CO2
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2. Principles of fluid therapy in post operative period [14]
Ans.
Indications
 For rapid restoration of fluid and electrolytes in
dehydration due to vomiting, diarrhoea, shock due to
haemorrhage or sepsis or burns.
 Total parenteral nutrition.
 Anaphylaxis, cardiac arrest, hypoxia.
 Post-GI surgeries.
 For maintenance, replacement of loss or as a special fluid .
Advantages: Controlled, accurate and adjustable, rapid and predictable
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1) Hyperkalemia [21, 12]
Ans.
is defined as existing when serum K+ is > 5 mmol/L.
Causes of HYPERkalaemia
 Haemolysis during venepuncture or in vitro – Release of intracellular K+
1) Artefactual during sample collection
 Thrombocytosis/leucocytosis
- Dietary Potassium
2) Increased intake
- Potassium-containing intravenous fluids
 Acidosis
3) Redistribution  Insulin deficiency & severe hyperglycaemia
From cells (flux of  β – blockers
K+ into PLASMA)  Hyperkalaemic periodic paralysis
 Rhabdomyolysis, Severe haemolysis & Tumour lysis syndrome
↓GFR – Acute kidney injury & chronic kidney disease
↓ Mineralocorticoid receptor activation – seen in:
Addison’s disease & Congenital adrenal hyperplasia
ACE inhibitors & ARBs {↓ Aldosterone levels}
Calcineurin inhibitors, Spironolactone & Eplerenone {block the
mineralocorticoid receptor}
4) Reduced urinary Heparin {inhibits aldosterone production}
excretion
↓ Renin production – can occur due to: NSAIDs & β-blockers
Tubulointerstitial diseases – Interstitial nephritis, Diabetic nephropathy &
Obstructive uropathy
Others:
 Amiloride – Blocks K+ exchange in distal tubule
 Gordon’s syndrome – ↓ K+ secretion in the renal tubules
Clinical features
⇨ Mild to moderate hyperkalaemia (< 6.5 mmol/L) is usually
asymptomatic
⇨ In severe cases muscular weakness & cardiac arrest occurs.
⇨ Electrocardiogram (ECG) changes: �
Management
 Treatment of hyperkalaemia depends on its severity
and the rate of development
 Mild to moderate hyperkalaemia (< 6.5 mmol/L) can be
treated with a reduction of potassium intake and
correction of predisposing factors
 Treatment of severe hyperkalaemia �

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2) Metabolic Alkalosis [12]
Ans.
Definition: Metabolic alkalosis is characterized by
an increase in extracellular pH above 7.45 due to
primary increase in plasma bicarbonate
Pathogenesis:
Loss of HCl by vomiting or nasogastric suction
production of acid by
stomachgeneration of bicarbonate.
Fluid loss by vomiting or nasogastric suction
promotes proximal tubular reabsorption of Na+,
HCO3- in exchange for K+ and H+ in distal
nephron
Severe hypokalemia causes metabolic alkalosis
by shifting hydrogen ions into the cells.
Clinical features:
Symptoms of alkalosis – hypoventilation, confusion, altered mentation and coma.
Severe alkalemia increases calcium levels resulting in numbness tingling sensation or tetany
Chloride responsive metabolic alkalosis have symptoms related to volume depletion  thirst and
lethargy.
Chloride unresponsive metabolic alkalosis causes symptoms related to hypertension
Severe hypokalemia can lead to arrhythmias
Management
Identify & treat the cause
Most cases respond to volume repletion – Normal saline + potassium chloride is the fluid of choice
In severe cases resistant to volume repletion – Ammonium chloride or arginine hydrochloride can
be used.
Chloride responsive metabolic alkalosis responds to volume resuscitation and chloride repletion.
----------------------------------------------------------------------------------------------------------------------------------------
3) Sodium Depletion / Hyponatremia [07, 06]
Ans.
 Hyponatremia is defined as serum sodium <
135 mEq/L
Treatment:
Symptomatic hyponatremia or severe
hyponatremia (Na <120 mEq/L) is treated with
immediate bolus of 4–6 mL/kg of 3% sodium
chloride.
Sodium levels have to be corrected gradually
over a period of time.
Rapid correction should be strictly avoided in
order to prevent Central Pontine Myelinolysis (CPM).
Hyponatremia induced seizures respond poorly to anticonvulsants.
SIADH – fluid restriction + Furosemide
Cerebral salt wasting – High-dose fludrocortisones (0.2–0.4 mg/day) is tried
1. Enumerate causes of Vaso-occlusive diseases. Describe thromboangiitis obliterans – Etiology, C/F,
inv. & Mx [15]
a. Berger's Disease [21, 04, 02]
b. Describe causes, clinical features, inv. & Mx of acute ischaemia of the lower limb [14, 11]
c. Lumbar Sympathectomy [07]
Ans.
Causes of Vaso-occlusive diseases: �

It is segmental, nonatherosclerotic inflammatory

disease of small & medium sized vessels with
cell mediated sensitivity to type I and type III
collagen
:
Risk factors: male smokers with SI>300, hypersensitivity to cigarette, Lower socioeconomic group,
recurrent minor feet injuries, poor hygiene
Arterial lumen is blocked but not thickened like atherosclerosis
Smoke contains carbon monoxide & nicotinic acid  Carboxyhaemoglobin  vasospasm and
hyperplasia of intima  Thrombosis obliteration of vessels  Eventually artery, vein and nerve
are together involved  Nerve involvement causes rest pain  plenty of collaterals open up
depending on the site of blockage  compensatory PVD  If patient continues to smoke, even
collaterals get blocked {decompensatory PVD – aka critical limb ischaemia}  rest pain, ulceration,
gangrene.
: it is a smoker’s disease 7Ps
 Intermittent claudication in foot and calf progressing to rest pain, ulceration, gangrene
 Recurrent migratory superficial thrombophlebitis
 Absence/Feeble pulses distal to the block
 May present as Raynaud's phenomenon

Hemogram & Hb; Blood sugar, Lipid profile; ABPI.

Arterial Doppler and Duplex scan (Doppler+ B mode US).
Ultrasound abdomen – to see abdominal aorta for block/ aneurysm
CT angiogram – to plan the intervention – either transfemoral or transbrachial approach
Vein, artery, nerve biopsy

Stop smoking "opt for either cigarette or limb, but not both."
:
Analgesics & sedatives
Anti-lipid drugs like atorvastatin
Low dose of aspirin 75 mg once a day – antithrombin activity.
Cilostazole 100 mg bid – is a phosphodiesterase inhibitor which improves circulation
 – Buerger's position & exercise; Care of feet {Chiropody} – avoid trauma, apply
oil, heel raise;
– to achieve vasodilatation by injecting local anaesthetic (xylocaine 1 %,
phenol) paravertebrally beside bodies of L2, 3 and 4 vertebrae in front of lumbar fascia
:
Omentoplasty – to re-vascularise the affected limb. PILAO
Profundaplasty – if block is in profunda femoris artery – to open collaterals across the knee joint
Lumbar sympathectomy – to  cutaneous perfusion so as to promote ulcer healing.
Amputations – can be done depending on site, severity and extent of vessel occlusion.
Ilizarov’s method of bone lengthening helps in improving the rest pain and claudication by creating
neo-osteogenesis and improving the overall blood supply to the limb.
----------------------------------------------------------------------------------------------------------------------------------------

1) Abdominal aortic aneurysm [21, 17, 14, 10]

Ans.
AAA is a localised, progressive and permanent dilatation usually larger than 3 cm in diameter of the
abdominal aortic wall
: Atherosclerosis {MC}, Familial aortic aneurysm, Syphilis, dissection, trauma, collagen diseases,
infection, arteritis, cystic medial necrosis, association with Chlamydia pneumoniae etc.
:
Some cases are asymptomatic
It presents as back pain, abdominal pain, mass abdomen which is smooth, soft, nonmobile, not
moving with respiration, vertically placed above the umbilical level, pulsatile both in supine as well
as knee-elbow position with same intensity, resonant on percussion
Lower limb ischaemia and embolic episodes can occur.
GIT, urinary, venous symptoms can also occur
Aortocaval fistula & Aortoenteric fistula can also occur

Blood urea, serum creatinine

Blood sugar, lipid profile, ECG etc.
Imaging: USG, aortogram, CT scan, CT angiogram, MR angiogram.

: Retroperitoneal mass, pseudocyst of pancreas, retroperitoneal cyst, etc.

:
 Conservative/Medical Treatment: Risk factor modifications; stopping smoking; control of BP
(propranolol), cholesterol; usage of drugs – α blockers, elastase inhibitors (NSAIDs-indomethacin),
matrix metalloproteinases (MMP) inhibitor (doxycycline).
 Surgical Treatment – for large aneurysms (>5.5 cm), painful aneurysms etc.
Open surgical repair {endo-aneurysmorrhaphy with intraluminal graft placement}
Endovascular aneurysm repair (EVAR) – if aneurysm is <5 cm
For ruptured aneurysms – Dx by USG Resuscitation, Massive blood transfusions  Emergency
surgery  Aneurysm is excised and the arterial graft either PTFE (Polytetrafluoroethylene),
knitted Dacron graft, or woven Dacron graft is placed. The graft is sutured to the vessel above
and below using monofilament, nonabsorbable suture material, polypropylene 5-zero
----------------------------------------------------------------------------------------------------------------------------------------
2) Raynaud's syndrome / Disease / Phenomenon [21, 09]
Ans.
"Raynaud's phenomenon" is an episodic, localized, vasospasm of small vessels of hands and feet
that leads into temperature and colour changes with sequence of clinical features called as
'Raynaud's syndrome'
:
Raynaud's disease – seen in females; occurs due to abnormal sensitivity to cold;
Working with vibrating tools: Like pneumatic road drills, chain saws, wood cutting, fishermen
travelling in machine boats – vibration white finger
Collagen vascular diseases: Like scleroderma, rheumatoid diseases causing vasculitis (all
autoimmune diseases).
Other causes: Cervical rib, Buerger's disease, Scalene syndrome, CREST syndrome
: 2 – vasospastic & obliterative
:�
Peripheral pulses (radial/ulnar) are normally felt
Usually, medial 4 digits and palm are involved.
Thumb is spared.
:
Angiogram of hand, Duplex scan – to identify the type
X-ray of the part, ANA assay, other specific tests etc.
Special investigations: Assessment of segmental BP
gradient from brachial-forearm-wrist-fingers; fingertip
thermography; cold recovery time, reactive hyperaemia time etc.
Other routine tests for arterial diseases like blood sugar/lipid profile/hypercoagulability status
: Treat the cause.
Avoid precipitating factors – protect from cold, hand warmer, hand gloves, stop smoking. Avoid
vibrating tools.
Low dose aspirin (75-100 mg per/day), Steroids for secondary Raynaud's.
Vasodilators – ACE inhibitors, Calcium antagonist, nitrates, misoprostol (oral PGE1).
1 % topical glycerine trinitrate is useful.
Cervical sympathectomy – can be done for nonhealing digital ulceration.
Localized digital sympathectomy – stripping off the adventitia of digital vessels, radial and ulnar
arteries + resection of nerve of Henle (a branch of ulnar nerve in the forearm – is sympathetic
innervation of the ulnar artery) is said to be effective.
----------------------------------------------------------------------------------------------------------------------------------------
3) False aneurysms [15, 09]
Ans.
Pseudo or False aneurysms refers to a extravascular hematoma
communicating with the intravascular space following a wall defect
Example: Rupture of left ventricle, which complicates myocardial
infarction or hematoma that follows trauma to artery
False aneurysm is common in femoral artery – It is treated with thrombin
injection if size is <3 cm; if size is >3 cm surgical repair of artery + graft is indicated.
----------------------------------------------------------------------------------------------------------------------------------------
4) Angiography [13]
Ans.
Angiography is the investigation for arterial diseases
Femoral artery is used because it can be easily felt and
cannulated to pass an arterial catheter
Seldinger technique is commonly used for angiogram
Interpretations:
 Cork screw appearance – in TAO
 String of beads – in Fibromuscular dysplasia
 Puff of smoke appearance – in Moya Moya disease
----------------------------------------------------------------------------------------------------------------------------------------
5) Intermittent claudication [07]
Ans.
Intermittent claudication refers to a crampy pain in the limb muscles.
Pathogenesis: Due to arterial occlusion  anaerobic muscle metabolism  lactic acid & substance P
accumulate in the muscle and cause pain.
 The site of pain depends on site of arterial occlusion: The most common site is calf muscles {due
to occlusion of Superficial femoral artery}.
Criteria to diagnose intermittent claudication:
 Cramp like pain in a muscle (calf) .
 Pain develops only when muscle is exercised.
 Pain disappears when exercise stops within 5 minutes.

----------------------------------------------------------------------------------------------------------------------------------------
6) Emboli [06, 05]
a. Air embolism [14]
b. Embolectomy [10]
c. Peripheral arterial embolism [01]
Ans. Definition of Embolism: An embolus is a detached intravascular solid, liquid, or gaseous mass
that is transported in the blood to a site distant from its point of origin. Unless otherwise specified, emboli should be
considered thrombotic in origin and the process is known as thromboembolism

 Through venous access like IV cannula, MC cause.

 During artificial pneumothorax. During surgeries of neck and axilla.
 Traumatic opening of major veins sucking air inside, causing embolism.
 During fallopian tube insufflation; laparoscopic surgeries.
 During illegal abortion.
It causes respiratory distress, haemoptysis, convulsions, unconsciousness, visual
and hearing disturbances, fatigue and numbness, paralysis, haemodynamic instability and coma.
Patient is placed in Trendelenburg left lateral decubitus
position.

 Patient is placed in Trendelenburg left lateral decubitus position.

 Hyperbaric oxygen reduces the nitrogen from the bubble so that to improve perfusion and
oxygenation.
 Often requires life-saving open thoracotomy to aspirate the excess air causing the block.
Embolectomy
It is done as early as possible as an emergency operation.
Under fluoroscopic guidance, Fogarty catheter (interventional
radiology) is passed beyond the embolus and balloon is inflated.
Catheter is withdrawn out gently with embolus. Angiogram is
repeated to confirm the free flow.

Acute embolic blockade of artery commonly seen in common

femoral, cranial vessels, mesenteric vessels.
It should be done within 6 hours as after 6 hours irreversible
changes occur – Golden hour.
----------------------------------------------------------------------------------------------------------------------------------------
7) Berry aneurysm [2000]
Ans.
Berry Aneurysms: (Saccular Aneurysms): “MC type of intracranial aneurysm.”
Site: Anterior part of circle of Willis, near branch points
Risk factors: Cigarette smoking & hypertension
Etiology: Sporadic (MC) or developmental
Pathogenesis: Underlying defect in the media of the vessel promotes aneurysm formation.
Associations: Autosomal dominant PCKD; Neurofibromatosis type 1; Marfan syndrome
Complications: Rupture results in subarachnoid hemorrhage
----------------------------------------------------------------------------------------------------------------------------------------

1. Complications of aneurysm [13]

Ans.

----------------------------------------------------------------------------------------------------------------------------------------
2. Leriche syndrome [07]
Ans.
 Leriche Syndrome {aka aortoiliac occlusive disease}, is caused by severe atherosclerosis affecting
the distal abdominal aorta, iliac arteries, and femoro-popliteal vessels.
Leriche Syndrome presents with a triad of claudication, impotence, and absence of femoral pulses.
Claudication is seen in both buttocks, thighs, and calves;
Impotence occurs due to defective perfusion through internal iliac arteries and so into the penis
causing erectile dysfunction
Bruit over aortoiliac region can be heard.
----------------------------------------------------------------------------------------------------------------------------------------
3. Classification of Aneurysm [07]
Ans.

Classification Definition
True aneurysms Involve all the 3 layers of artery or the thinned wall of the heart.
Extravascular hematoma communicating with the intravascular
Based on
Pseudo or False space following a wall defect.
layers
aneurysms: Ex: Rupture of left ventricle, which complicates myocardial
involved
infarction or hematoma that follows trauma to artery
Saccular
aneurysms Spherical outpouchings involving only a portion of the vessel
Ex: Berry wall. They vary in diameter & often contain thrombus
Aneurysm
Fusiform It is ovoid or fusiform dilation of vessel wall that is parallel to the
Based on
aneurysms long axis. They vary in diameter & length.
gross
Cylindrical
appearance It has parallel dilatation
aneurysm
Arterial
dissection/ It develops when blood enters/dissects between the layers of the
dissecting arterial wall
hematoma
Congenital Berry aneurysms
Based on
due to Atherosclerosis & HTN (MC); Infection (Mycotic
Etiology Acquired:
aneurysms)
1) Define & Classify shock. Discuss classification, pathophysiology, clinical monitoring and Mx of
hypovolemic shock [20, 19, 16, 13, 09] Types of shock Pathophysiology Causes
a. Cardiogenic shock [12]
Massive
Ans. Loss of
hemorrhage,
Shock is defined as a state of cellular and blood/plasma/
1. Hypovolemic trauma, burns,
fluid → low
tissue hypoxia with either oxygen delivery shock Vomiting, diarrhea,
cardiac output →
oxygen utilisation increased oxygen severe
tissue ischemia
consumption with circulatory failure gastroenteritis
(collapse) and poor perfusion Myocardial
Myocardial infarction,
damage Myocarditis,
Classification: Ventricular rupture
1) Valvular failure
(stenosis or
2. Cardiogenic incompetence)
shock Mechanical 2) Hypertrophic
cardiomyopathy
Pathophysiology of hypovolaemic shock: 3
3) Ventricular
stages septal defect
Ventricular
Reflex compensatory mechanisms are Arrhythmic
arrhythmias
activated (e.g., Baroreceptor reflexes, catecholamine Endothelial
release, ADH release, RAAS and generalized sympathetic activation/injury; Microbial infections
stimulation) to redistribute the blood supply. 3. Septic shock leukocyte-induced (bacterial, fungal,
damage & DIC  viral, rickettsial).
widespread tissue hypoperfusion and vascular dilatation
hypoxia → anaerobic glycolysis → lactic 4. Neurogenic
Spinal Injury  loss of sympathetic tone
acidosis → ↓ tissue pH → dilatation of Shock
arterioles → peripheral pooling of blood occurs due to mechanical obstruction of
5. Obstructive circulation due to pulmonary embolism,
into the microcirculation → ↓ Cardiac
shock tension pneumothorax or cardiac
Output → anoxic injury to endothelial cell tamponade, aortic stenosis.
→ favours DIC → widespread tissue Anaphylactic shock; Distributive shock
6. Other types:
hypoxia → damage of vital organs etc.
: Injury is so severe that even if the hemodynamic defects are corrected, survival
is not possible because of multiorgan failure
Clinical monitoring of Hypovolaemic shock:
Regular monitoring of BP, pulse rate, respiratory rate & urine output should be done
Urine output should be more than 0.5 mL/kg/hour {catheterise to measure urine output}
Measure Central venous pressure & pulmonary capillary wedge pressure {to assess LV function}
Pulse oximetry; ABG analysis; LFT; RFT & coagulation profile should be done
CBP, ESR, pH assessment, serum electrolytes & chest X-ray (to rule out ARDS/pulmonary problems)
Serum lactate estimation – to detect tissue ischemia
Specific investigations – Ex: Pus/urine/blood/bile/sputum cultures; USG of the part, CT/MRI etc.
Management Aim is to treat the cause, to improve cardiac function and to improve tissue perfusion
 Initial acute critical care management using -Airway; -Bleeding; -Circulation; -Disability, drugs;
-Exposure should be done
Treat the cause, e.g., arrest haemorrhage
Fluid replacement – via NS; RL; Plasma expander (haemaccel) (max. 1L can be given in 24 hours)
Blood transfusion in severe cases.
Ranitidine IV or omeprazole IV or pantoprazole IV
{for stress ulcers}
To improve cardiac function:
 Give inotropes – Ex: Dopamine, dobutamine,
adrenaline infusion etc.
 Put in Trendelenburg’s position
 MAST (military antishock trouser) – it is wrapped around lower limb & abdomen to redistribute
the existing blood and fluid towards centre
To improve tissue perfusion –
 Nasal oxygen to improve oxygenation
 Correction of acidosis - by using 8.4% IV sodium
bicarbonate.
 Steroid – Ex: hydrocortisone
 Antibiotics in patients with sepsis
 Haemodialysis may be necessary when kidneys are not functioning
----------------------------------------------------------------------------------------------------------------------------------------

1) Septic shock [18, 10, 02]

Ans.
Septic shock is a vasodilatory shock which is resistant to
vasopressors.
It occurs due to toxin-induced release of isoform of nitric oxide synthetase from the vessel wall
nitric oxide.
: Microbial infections (bacterial, fungal, viral, rickettsial, protozoal).
Gram-negative septic shock is called
as endotoxic shock
 – {refer 1st LQ}
Appropriate antibiotics – third generation cephalosporins/ aminoglycosides.
Pus/urine/discharge/bile/blood culture and sensitivity for antibiotics
Treat the cause or focus – drainage of an abscess; laparotomy for peritonitis; resection of
gangrenous bowel; wound excision etc.
Activated C protein prevents the release of inflammatory mediators
Monitoring the patient by pulse oximetry, cardiac status, urine output, arterial blood gas analysis.
----------------------------------------------------------------------------------------------------------------------------------------
2) Central Venous Pressure (CVP) [11]
Ans. Central venous pressure or right atrial pressure is the measurement of
pressure at the junction of superior vena cava and right atrium
 It is a measure of right ventricular preload & also the blood volume status
in body
 Normal value: 5–12 cm H2O.
 Subclavian vein or internal jugular vein are used for cannulation for
central line and CVP measurement (Subclavian route is preferred).

 Clinical method – measure the JVP height in a patient positioned in semi reclined position.
 Other bedside method – CVP manometer connected to
a central line.

To guide fluid therapy

Guide use of vasopressors and colloid infusions
Diagnoses of arrhythmias – Ex: in atrial fibrillation, the
‘a’ wave of CVP disappears and ‘c’ wave becomes taller
Diagnoses of tricuspid valve lesions (regurgitation or
stenosis), pulmonary HTN, pulmonary valve stenosis
----------------------------------------------------------------------------------------------------------------------------------------
3) Systemic Inflammatory Response Syndrome (SIRS) [09]
Ans.
SIRS is a final common pathway in shock due to any
cause, infectious or non-infectious (pancreatitis,
polytrauma, burns, transfusion reaction, and
malignancy) where there is failure of inflammatory
localisation with vasodilatation, endothelial
permeability & damage, thrombosis, leucocyte migration and activation.
SIRS is a part of severely decompensated reversible shock which eventually leads to MODS
(Multiorgan dysfunction syndrome), a state of irreversible shock wherein patient is anuric, drowsy,
cold and terminally ill.
SIRS carries poor prognosis.
1. Varicose veins of LL – Surgical Anat, etiopath, C/F, Complications, inv. & Mx [18, 16]
a. How will you examine, diagnose, investigate and treat varicosity of the long saphenous venous
system? [04]
Ans.

: It is permanently elongated, dilated vein/veins with tortuous path causing pathological

circulation. There is reversal of blood flow through its faulty valves
:
Risk factors: heredity; female sex; obesity, occupation that demands prolonged standing;
immobility; intra-abdominal pressure like in sports, tight clothing, pregnancy, raised
progesterone level, chronic constipation, high heels etc.
Primary varicosities occur due to Congenital incompetence or absence of valves
Secondary varicosities occur secondary to other causes {pregnancy, long standing etc.}
Pathogenesis can be explained by 2 theories:
Fibrin cuff theory: Incompetence of venous valves  Stasis of blood  Chronic ambulatory
venous hypertension  RBC diffuses into tissue planes  Lysis of RBC's & release of
haemosiderin  Pigmentation & Dermatitis  Capillary endothelial damage  Prevention of
diffusion and exchange of nutrients  Severe anoxia  Chronic venous ulceration
White cell trapping theory: Inappropriate activation of trapped leucocytes  release proteolytic
enzymes  cell destruction and ulceration
:
Saphena varix – a large varicosity in the groin which becomes
visible and prominent on coughing
Brodie-Trendelenburg test – to know saphenofemoral
incompetence {Trendelenburg-I} & Perforator incompetence
{Trendelenburg-II}
Perthe’s test – to assess for DVT
 Three tourniquet test – To find out the site of incompetent
perforator, 3 tourniquets are tied after emptying the vein at
saphenofemoral junction, Above knee level & below knee
level
Other tests: Schwartz test, Fegan's test, Pratt's test,
Morrissey's cough impulse test & Ian-Aird test
Examination of the abdomen has to be done to look for pelvic
tumours, lymph nodes, which may compress over the veins to
cause varicosity
:
Venous Doppler at SPJ & at perforators – it also helps to know
DVT
Duplex scan – for proper venous haemodynamic mapping
Plethysmography – to measure volume changes in legs
Ultrasound abdomen, peripheral smear, platelet count etc.
can be done depending on the cause of varicose veins
:
Conservative treatment:
 Elevation of the limb - relieves oedema
 Elastic crepe bandage application from below upwards or use of pressure stockings to the limb
 Other options: Unna boots, Pneumatic compression methods etc.
Drugs used for varicose veins:
 Calcium dobesilate: 500 mg BD – to improves macrophage mediated proteolysis &  oedema
 Troxerutin 500 mg BD – Anti-erythrocyte aggregation agent which improves capillary dynamics
 Diosmin – to protects venous wall and valve – it is anti-inflammatory, profibrinolytic, anti-oedema,
lymphotropic
Injection-sclerotherapy – indicated in Uncomplicated
perforator incompetence or aged/unfit patients – STDS {sod.
tetradecyl sulphate 3%} sclerosant is commonly used.
Surgical options:
Trendelenburg operation (Crossectomy)
Stripping of vein using Myer's stripper
Ligation of short saphenous vein at sapheno-popliteal junction
Minimally invasive methods – Ex: Subfascial endoscopic perforator ligation
surgery (SEPS); Radiofrequency ablation (RFA) method; Endovenous laser
ablation (EVLA) etc.
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1) Deep vein thrombosis (incl Complications) [21, 19, 11, 03]

a. Prophylaxis for Deep vein thrombosis [11]
b. Thrombosis [04]

Ans. is called as phlebothrombosis. It is semisolid

clot in the vein which has got high tendency to develop pulmonary embolism and sudden death
: 3 abnormalities can lead to formation of a thrombus {Virchow’s triad}
1) Endothelial Injury Platelets adhere to the site of endothelial injury and release prothrombotic
tissue factor. It can be either due to physical damage or endothelial dysfunction
a) Physical Damage:
 To Heart: Due to MI, Catheter trauma, endocarditis etc.
 To Blood Vessels – Ex: Ulcerated atherosclerotic plaques,
Vasculitis & DIC
b) Endothelial Dysfunction:
- Causes: Hypertension, turbulent blood flow, toxins (e.g.,
endotoxins, cigarette smoke), radiation injury, metabolic
abnormalities (e.g., homocystinemia or hypercholesterolemia).
2) Alterations in Normal Blood Flow:
 Causes: Turbulence (produce thrombus in the arteries and heart)
& Stasis (major cause for venous thrombosis).
 Clinical disorder associated with turbulence and stasis:
• In Heart: Acute MI, Arrhythmias & Dilated cardiomyopathy.
• In Arteries: Ulceration of atherosclerotic plaques & Aneurysms
• Varicose veins.
• Hyper viscosity – Ex: Polycythemia Vera
• RBC disorders- Ex: sickle cell anemia
3) Hypercoagulability (thrombophilia): �
: Leg veins – esp. veins of soleus muscle in calf
: Commonly it is asymptomatic
 Fever-earliest symptom
 Severe pain and swelling in the calf and thigh (often).
 Positive Haman's sign: Passive forceful dorsiflexion of the foot with
extended knee will cause tenderness in the calf
 Mose's sign: Gentle squeezing of lower part of the calf from side-to-side is painful.
 Neuhof's sign: Thickening and deep tenderness elicited while palpating deep in calf muscles
 Features of pulmonary embolism: chest pain, breathlessness and haemoptysis
: Ruptured Baker's cyst; Ruptured plantaris tendon; Calf muscle haematoma; Cellulitis leg;
Superficial thrombophlebitis.
:
Venous Doppler with Duplex scanning – shows noncompressible vein which is wider than normal
Venogram & Radioactive I125 fibrinogen study can also be done
Haemogram with platelet count, D-dimer test & analysis of fibrin degradation products (FDP)
Investigations for pulmonary embolism: pulmonary artery CT scan with filling defect; pulmonary
angiography & Ventilation-perfusion scanning
:
Rest, elevation of limb, bandaging the entire limb with crepe
bandage
Anticoagulants – low molecular weight heparin; warfarin – for fixed
thrombus
Fibrinolysin – Streptokinase – for free thrombus
Venous thrombectomy can be done using Fogarty venous balloon catheter.
IVC filter {intracaval filters} – to prevent thrombotic emboli from reaching the heart
----------------------------------------------------------------------------------------------------------------------------------------
2) Haemangioma (incl types & Mx) [05, 99]
 a. Capillary Hemangioma [21]
b. Cavernous Hemangioma [16]
Ans.
Haemangioma is a benign vascular endothelial tumour, common in girls
:2�

Maffucci syndrome: cavernous

haemangioma + dyschondroplasia
Kasabach Merritt syndrome: Capillary
haemangioma + DIC with
thrombocytopenia
: Lymphangioma; Lipoma, cold
abscess, lymph cyst
: Ultrasound, Doppler; CT
angiogram to find out feeding vessel;
Platelet count; MRI/MR angiogram to see
feeding vessels and deeper extension
: Haemorrhage; DIC;
Thrombosis; Infection, ulceration and
septicaemia; Erosion into the adjacent
bone; High output cardiac failure
----------------------------------------------------------------------------------------------------------------------------------------
3) Venous ulcer [05, 99]
a. Bisgaard’s method of treatment of varicose ulcer [10]
Ans.
It is the complication of varicose veins or deep vein thrombosis
Etiopathogenesis: Ambulatory venous hypertension is the
prime cause of venous ulcer formation �
Clinical presentations:
Common site: Gaiter’s zone {around and above the medial
malleoli} because of presence of large number of perforators
Ulcer is often large, nonhealing, tender, recurrent with
secondary infection
Vertical group of inguinal lymph nodes are enlarged and tender
Most of the venous ulcers have surrounding lipodermatosclerosis {Champagne bottle sign/inverted
beer bottle sign}
Talipes equinovarus – Due to regular walking on toes so as to relieve the pain
DDx: ischaemic ulcer, diabetic ulcer; Rheumatoid ulcer; Traumatic ulcer; Neuropathic ulcer;
Neoplastic ulcer
Investigations:
Discharge from the ulcer for culture and sensitivity
X-ray of the area to look for periostitis
Venous doppler
ESR, CRP, peripheral smear; red cell counts
Wedge biopsy from the ulcer edge to rule out Marjolin's ulcer.
Investigations to rule out other causes of leg ulcers like arterial; neurological; diabetes; sickle cell
disease and other haemolytic diseases
Treatment:
Bisgaard method – elevation, massage & exercise – to edema, venous drainage & promote ulcer
healing
Care of ulcer – regular dressing with povidone iodine
Four-layer bandage technique to achieve high compression pressure.
Specific treatment tor varicose veins – Trendelenburg operation, stripping of veins & perforator
ligation
1. Hemorrhage – Define and classify; physiological and pathological effects; Treatment [21, 17, 13, 07]
Ans.
: Hemorrhage is defined as the escape of blood outside its containing vessel

Based on the source

Arterial, Venous & Capillary
of bleeding
a. Primary: Occurs at the time of injury or operation.
Based on the time
b. Reactionary – occurs within 24 hours after surgery or after injury
of onset of bleeding
c. Secondary: It usually occurs in 14 days after surgery.
Revealed; Concealed (internal hemorrhage);
Based on visibility
Initially concealed but later revealed – Ex: Melaena; Haematemesis
a. Acute haemorrhage – sudden, severe haemorrhage after trauma, surgery.
b. Chronic haemorrhage: It is chronic repeated bleeding for a long
Based on the
period like in haemorrhoids, bleeding peptic ulcer etc.
duration of
c. Acute on chronic haemorrhage: It is more dangerous as the bleeding
haemorrhage
occurs in individuals who are already hypoxic, which may get
worsened faster
Based on the a. Surgical haemorrhage can be corrected by surgical intervention.
possible b. Nonsurgical haemorrhage--is diffuse ooze due to coagulation
intervention abnormalities and DIC.

Control of Haemorrhage by ressure; acking;

osition and Rest
- Local haemostatic agents: Gelatin sponge;
Collagen sponge; Topical thrombin; topical
cryoprecipitate etc.
End Points of Resuscitation:
keep the patient warm;
Prevention of further
coagulopathy (via fibrinogen infusion)

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2. Write in detail about blood transfusion [06]
a. Complications of blood transfusion [21, 19, 16, 12, 10]
b. Massive blood transfusion [21]
c. Indications of blood transfusion [20, 18]
d. Enumerate the various blood products. Discuss the indications, complications and their
treatment following blood transfusion [08]
Ans:

:
 Donor should be fit without any infections like HIV, hepatitis and malaria.
 Weight of donor should be more than 45 kg.
:
Whole blood – metabolically more active & is rich in coagulation factor;
- Disadvantage is that volume overload can occur
Packed RBCs – SAG-M (Saline, Adenine, Glucose-Mannitol) is used to store packed RBCs
Fresh-frozen plasma – 1st line therapy in fluid resuscitation in trauma associated coagulopathy
Cryoprecipitate – Supernatant of fibrinogen
Platelets – for patients with bleeding disorders
Prothrombin complex concentrates - Factor 2, 9 and 10 – Used to treat warfarin overdose
Autologous blood – patients undergoing elective surgery pre-donate their own blood up to 3
weeks before surgery for re-transfusion during the operation
After grouping and cross-matching, 540 ml of blood is transfused in 4 hours (40 drops per minute),
using a filtered drip set
Massive blood transfusion:
Definition: It is defined as replacement or transfusion of blood equivalent to patient's blood
volume in <24 hours corresponding to that particular age {In adult it is 5-6 litres, in infants it is 85
ml/kg body weight) or single transfusion of blood > 2,500 ml continuously.
Indications:
 In cases of severe trauma associated with liver, vessel,
cardiac, pulmonary, pelvic injuries
 During surgical bleeding (primary haemorrhage on table)
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1) Blood grouping and cross matching [13]

a. Transfusion reactions [15]
Ans.
During blood transfusion, only compatible blood must be used.
The one who gives blood is called the ‘donor’ and the one who receives the blood is called
‘recipient
 Blood matching (typing) is a laboratory test done to determine the blood group of a person.
Cross-matching is done when the typed blood is needed for transfusion
Cross-matching is always done before blood transfusion
While transfusing the blood, antigen of the donor and the are
considered
Cross-matching is done by mixing the serum of the recipient and the RBCs of donor;
Cross-matching = Recipient’s serum + Donor’s RBC
If agglutination of RBCs from a donor occurs during cross-matching, the blood from that person
is NOT used for transfusion to avoid transfusion reactions

This usually refers to an acute haemolytic reaction following incompatible blood transfusion.
There will be potentially fatal complement-mediated intravascular haemolysis and multiple organ
failure.
Febrile transfusion reactions are non-haemolytic and are usually caused by a graft-versus-host
response from leukocytes in transfused components.
Management: The blood transfusion should be stopped immediately.
----------------------------------------------------------------------------------------------------------------------------------------
2) Venesection [11]
Ans.
Venesection
(Phlebotomy) is the
act of drawing or
removing blood
from the circulatory
system through a
cut (incision) or
puncture for the
purpose of analysis,
blood donations or treatment for blood disorders
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1. Reactionary haemorrhage [15, 10, 06]

Ans.

Reactionary haemorrhage occurs within 24 hours after

surgery or after injury (commonly in 4-6 hours).

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2. Secondary haemorrhage [15]
Ans.

It usually occurs in 14 days after surgery.

1) Define burns. Enumerate the different causes of burns. Discuss the management of a 35 years old
female with 40% partial to full thickness burns [21]
a. Classification of Burns [20, 19]
b. Burns – Pathophysiology; C/F; Assessment & Mx [18, 14, 05, 04, 03]
c. Facial burns [02]
Ans.
: Burn is an injury caused by heat/ chemicals / electricity/ radiation producing coagulative
necrosis of tissues
{Etiological Classification}:
Thermal burns—due to fire, heat, bomb blasts, etc.
Chemical burns—due to acidic or basic chemical Pathophysiology of Burn Injury
such as hydrofluoric acid etc.
Electrical burns
Radiodermatitis – due to ionising radiation
Cold burns – Ex: Frost bite; Chilblain; Trench foot;

 History of burn.
 Pain, burning, anxious status, tachycardia, tachypnoea, fluid loss.
 Features of shock in severe degrees of burn.
:
Wallace's rule of nine – MC used for all patients
greater than 4 years of age�
Lund and Browder chart – used in children upto 4 years of age
Berkow formula is also useful in children.
:
Prehospital care – Extinguish the fire burning on a person; Cool the burn wound
with running tap water; Give oxygen; Elevate the burned limb
Follow ATLS protocol – ABC
– early elective intubation if indicated {trapped in smoke; change in voice etc.}
– nebulisers and warm humidified oxygen; look for metabolic poisoning
(due to CO) & any mechanical block to breathing from the eschar of chest wall
 – maintain fluid, electrolyte and acid base status
Oral fluids – for burns <10-15% TBSA; or else give IV fluids using Parkland formula
Parkland formula: Fluid requirement in ml = 2 x TBSA x Body weight(kg)
- The value obtained is divided into 2 parts with half given in first 8 hours and the remaining
given in next 16 hours
Other formulas for crystalloids – Moore formula, Brooke’s formula etc.
Management of the burn wound
For partial thickness wounds - Antiseptic cream impregnated dressings
 Antiseptic creams – Ex: Mafenide acetate; Silver sulphadiazine; Silver nitrate etc.
For full thickness burns  Escharotomy
Early excision of the burnt tissue followed by skin grafting
Look for Signs of compartment syndrome – 5Ps {pain, paraesthesia, pallor, pulselessness & pressure}
Other measures: Tetanus prophylaxis; Stress ulcer (curling ulcer) prophylaxis; Antibiotic
prophylaxis; DVT prophylaxis; Adequate analgesia & regular monitoring in ICU.
Nutrition: For a patient with > 40% TBSA burns, about 2000 kcal/ body surface area/ day is
required with 20% of calorie requirement being given through protein
Psychological support
----------------------------------------------------------------------------------------------------------------------------------------

1. Electrical burns [16, 15, 09]

Ans.

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1. Escharotomy [07]
Ans. Eschar is circumferential full thickness burn that can lead to compression
of the blood supply of a limb.
Eschar is insensitive, with thrombosed superficial veins.
Escharotomy – deep longitudinal incisions are made to prevent collection of oedema fluid and also
to prevent compression over the vessels. Can be done without anesthesia as the area is insensate
Indication of Escharotomy – Circumferential deep 2nd degree, 3rd degree & 4th degree burns with
impending or established compartment syndrome in chest/abdomen/limbs
Escharotomy causes large quantity of blood loss and so blood transfusion is needed while doing
escharotomy.
1) How will you investigate and manage a case of
Polytrauma? [05]
a. Triage [16, 11]
Ans.
refers to severely injured patients with
two or more severe injuries in at least two areas of the body

Triage means "To sort" in French.

Triage is a system to manage mass casualties. It aims to
identify the patients who will benefit the most by being
treated the earliest
By sorting out the minor injuries, triage lessens the
immediate burden on medical facilities
:

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1. Blunt Trauma Abdomen [21]

Ans:
It is common in accidents & is often missed or lately diagnosed.
Features of Blunt Trauma
 Signs of profound shock, progressive distension of abdomen, pain, tenderness, guarding, rigidity,
rebound tenderness, dull flank.
 Features specific of individual organ injury like obliteration liver dullness in bowel injury.
 Bruising of skin over the abdomen – London's sign.
 Respiratory distress, cyanosis.
 Repeated clinical examination is a must in blunt trauma.
Evaluation: Ultrasound Abdomen; CT Scan of Abdomen; Abdominal diagnostic paracentesis etc.
Management:
Evaluate the extent of injury, number of organs injured etc.
Exploratory laparotomy: After opening abdomen  control the profuse bleeding using finger
compression or mop or pressure  Individual organs are assessed & managed accordingly
 Resection or repair approach is decided depending on the severity of individual organ injury –
duodenum, pancreas, liver, spleen, bowel, kidney, etc.
Alternative: Persistent pressure mop in situ with closure of the abdominal wall with an option of
second look surgery in 48 hours
Management as critical care (ICU with intensivist); multiple blood transfusions; management of
sepsis, electrolyte changes, treatment of renal failure, provision of nutrition, prevention of DVT
should be done post-operatively
----------------------------------------------------------------------------------------------------------------------------------------

1) Abdominal Paracentesis [11]

Ans.
Abdominal paracentesis is a bed side clinical procedure in which needle is inserted into peritoneal
cavity & the fluid is removed
:
a) Diagnostic – small quantity of fluid is
removed for testing
b) Therapeutic: >5 litres of fluid is removed to
reduce intraabdominal pressure and relieve
the associated symptoms like abdominal
pain, dyspnoea etc.
: Pt with DIC; Distended bowel; Infections etc.
Rectus sheath haematoma.
1. Acute lymphangitis [15, 04]
Ans.
Acute lymphangitis refers to acute inflammation of the lymphatics occurs after bacterial infection
like Streptococcus pyogenes and Staphylococcus aureus.
It is common infective conditions of limbs.
:
Diffuse swelling in the skin with redness which blanches on pressure is typical.
Fever, chills, pain and tenderness
Regional lymph nodes are palpable & tender; abscess in the area can occur
Infection spreads faster especially in diabetics & immunosuppressed people septicaemia.
: DVT & Cellulitis
: Total count will be raised; blood sugar should be assessed. Ultrasound with venous
Doppler is done
:
Antibiotics oral or intravenous; NSAIDs
Limb elevation;
Glycerine magnesium sulphate local application;
If suppuration occurs  incision and drainage or fasciotomy + wound debridement.
If septicaemia develops critical care treatment is required after admission.
: Recurrent infection; development lymphoedema; septicaemia; lymphadenitis
----------------------------------------------------------------------------------------------------------------------------------------
2. Lymphoedema [09]
a. Endemic elephantiasis (Podoconiosis) [18, 14]
Ans.
Lymphoedema refers to accumulation of fluid (lymph) in
extracellular and extravascular fluid compartment, commonly
in subcutaneous tissue
: it occurs due to defective lymphatic drainage

:
Swelling in the foot, extending progressively in the leg – tree trunk pattern leg.
Buffalo hump in the dorsum of the foot; Squaring of toes
Initially pitting oedema occurs, which later becomes nonpitting.
 Stemmer's sign – Skin over dorsum of foot cannot be pinched because of subcutaneous fibrosis.
Dull ache/severe pain/burning/bursting/cramps
Debility/immobility/obesity/muscle wasting
Endemic elephantiasis (Podoconiosis):
Lymphoedema seen in barefoot workers due to
destruction of lymphatics by silica derived from soil
containing alkaline volcanic rocks {Africa}
No virus, bacterium or parasite identified
:
Skin thickening, abscess and maggot's formation
Recurrent cellulitis, non-healing ulcers, septicaemia
Lymphangiosarcoma/Stewart Treves syndrome – in
upper limb after mastectomy
Recurrent streptococcal infection
: Cardiac causes, hypoproteinaemia, malnutrition, liver failure, Myxoedema, lipoedema, Drugs
{steroid, estrogens, nifedipine}
:
: Limb elevation, Exercise; Weight Reduction; avoid prolonged standing;
 Pain relief – {avoid NSAIDs as it may precipitate necrotizing fasciitis}
 Benzopyrones – proteolytic agents; increase the lymphatic
peristalsis
 Below knee stockings – to edema
 Multi-layered lymphoedema bandaging (MLLB) – to edema
 Avoid trauma and infection; regular washing to keep the
limb clean
 Antibiotics & Topical antifungals
 Complex decongestive therapy & Manual lymphatic
drainage
:

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3. Hodgkin's Lymphoma [04, 02]  refer Medicine – Paper-I pg. No. 41
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1) Lymphangioma [08, 04]

a. Cystic Hygroma [19, 14, 13, 99]
Ans.
 It is congenital localised clusters of dilated lymph sacs in the skin and subcutaneous tissue that has
failed to join the normal lymph system during development period
 Types: Capillary Lymphangioma, Cavernous Lymphangioma & Cystic Hygroma
 Cystic Hygroma (Cavernous Lymphangioma) is a cystic swelling due to sequestration of a portion
of jugular lymph sac from the lymphatic system, during the developmental period in utero.
It is also called as hydrocoele of the neck
Lymphatics fail to communicate to venous system; abnormal budding of lymphatics is seen.
Often it is associated with Turner's, Down's, Klinefelter syndromes and trisomy 18 and 13.
 :
 Swelling is present at birth in the posterior triangle of neck {MC} causing obstructed labour.
 Swelling is smooth, soft, fluctuant (cystic), partially compressible, brilliantly transilluminant. It is
not reducible completely
 Disfigurement of face of the child
 Swelling may rapidly in size causing respiratory obstruction
 Rupture with lymph ooze can occur
:
• Aspiration of the contents with Pre-op injection of sclerosants (OK-432, PICIBANIL, Pure ethanol
etc.) and later once fibrosis develops  excision of entire aggregation of cysts
• When it causes respiratory obstruction, aspiration and tracheostomy is done.
----------------------------------------------------------------------------------------------------------------------------------------
2) Chyluria [07]
Ans.
It is passage of milky white chylous urine, which is aggravated after fatty meal.
: Occurs due to obstruction of intestinal lymphatic vessels  diversion of lymph into renal
lymphatics or it often may be due to rupture of intestinal lymphatics into renal pelvis or ureter
leading into a lymphourinary fistula.
 Cause of Obstruction: filarial (MCC); tumour, tuberculosis, malaria and ascariasis infestation.
: Clot colic due to lymph clot in urinary system may be the presentation.
: Urine study, culture, IVU, lymphangiography, U/S abdomen is needed.
is low fat, protein rich diet, antibiotics, DEC, plenty of oral fluid intake, ligation of dilated
lymphatics through laparotomy or sclerosing the lymph vessels.
1. Felon [13, 09]
a. Pulp space infection [05, 2000]
b. Pulp space infection of finger [03]
Ans.

Causative organism – bacteria – Staphylococcus {MC}; Streptococcus, Gram-

negative organisms
It is the second most common hand infection
Mode of injury - Usually by a minor injury like finger prick
Clinical Features:
 Index and thumb are commonly affected
 Pain, tenderness, swelling in the terminal phalanx suppuration  collar stud abscess
 Fever, tender axillary lymph nodes.
Investigations:
 X-ray of the part – to r/o osteomyelitis of terminal phalanx;
 Pus for culture and sensitivity to be sent.
Treatment: Antibiotics and analgesics are started.
----------------------------------------------------------------------------------------------------------------------------------------
2. In-growing toe nail [11]
Ans.
(aka In-growing toe nail or embedded toe nail).
 Occurs due to curling of the side of nail inwards, causing it to form a lateral
spike resulting in repeated irritation and infection of overhanging tissues in
the nail fold.
Tight shoes; Improper cutting of nails (very short and convex).

 It is common in great toe and is often bilateral.

 Both medial and lateral sides of the toe can be involved.
 Recurrent attacks of paronychia (nail infection) occurs.
 Pain, tenderness, swelling of margins of the toe, often along with granulation tissue and foul-
smelling discharge.

 Zadik-Fowler's radical nail excision with flap elevation at

angles
 Regular dressing and packing; Antibiotics.
 Discharge is sent for culture and sensitivity.
Prevention: Nails should be cut concavely or straight
without leaving lateral spikes towards soft tissues.
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3. Compound palmar ganglion [09]
Ans.
It is chronic tenosynovitis of flexor tendon sheaths due to tuberculosis (tuberculous tenosynovitis) or
rheumatoid arthritis.
Site: Flexor tendon sheath on either side of the wrist is involved
Swelling contains fluid with typical melon seed bodies.
Swelling is smooth, soft, nontender, fluctuant and also cross-
fluctuant across flexor retinaculum, non-transilluminating.
Wasting of hand and forearm muscles are seen.
Primary focus may be present in lungs.
:
ESR, chest X-ray, MRI hand.
FNAC of axillary lymph node and swelling itself.

Start anti-tuberculous drugs

Excision of flexor tendon sheath + scraping of caseating material &melon seed bodies.
Care should be taken not to injure median and ulnar nerves.
----------------------------------------------------------------------------------------------------------------------------------------
4. Infections of the Hand [05]
Ans.
Hand contains neurovascular bundles, muscles, bones and ligaments.
 Infection may be due to minor injuries or blood borne.
Precipitating causes: Diabetes; immunosuppression; Trauma; HIV
infection; Steroid therapy; vascular diseases.
Causative Organisms: Staphylococcus aureus (MC); Streptococcus
Gram-negative organisms like E. coli, Klebsiella.
General Features of Hand Infection
Infection spreads faster with fever, severe pain and tenderness
Looks like frog hand – oedema over the dorsum of hand due to lax
skin and more lymphatic network.
Restricted movements of fingers and hand.
Tender palpable axillary lymph nodes are often present.
Investigations: Pus for culture and sensitivity; Blood sugar; Urine sugar and ketone bodies; X-ray of
the part; Arterial Doppler of the hand if needed.
Management
 Antibiotic therapy.
 Incision and Drainage of localised pus – Draining incision should not cross the palmar crease.
Use tourniquet to create Bloodless field while draining the pus
Care should be taken not to injure neurovascular bundles.
Pus should be sent for culture and sensitivity.
 Post-op measures:
 Rest the hand in glass-holding position
 Elevation of hand reduces the oedema, increases perfusion, promotes healing
 Physiotherapy and regular exercise of hand and fingers
----------------------------------------------------------------------------------------------------------------------------------------
5. Paronychia [04]
a. Acute Paronychia [14]
Ans.
Paronychia is a term used to describe nail infection
It is the most common hand infection
Site: Paronychia occurs in subcuticular area under the eponychium.
Etiology:
 Minor injury to finger will inoculate the bacteria.
 Causative organisms: Staphylococcus aureus and Streptococcus pyogenes
Clinical Features: Severe throbbing pain and tenderness {dependent
throbbing) with visible pus under the nail root. Nail on touch is very tender
Management:
 Pus is drained by making an incision over the eponychium
 Pus is sent for culture and sensitivity.
 Antibiotics – cloxacillin, amoxicillin & Analgesics.
 If there is a floating nail, then the nail is dead and it has to be removed.
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6. Deep space infections of the hand [02]
Ans.
Two deep palmar spaces are present:
1. Mid-palmar space. 2. Thenar space.
Causes:
Trauma
Spread from infection of finger spaces and web spaces
Clinical Features
Pain and tenderness in the palm – Painful movement of
metacarpophalangeal joint (but interphalangeal joint
movements are normal and pain free).
Oedema of dorsum of hand (frog hand).
Loss of concavity of palm.
Fever & Palpable tender axillary lymph nodes.
Eventually pus may come out of palmar aponeurosis forming
collar stud abscess and later sinus formation.
X-ray of the part is required.
Treatment:
Elevation of the affected limb
Antibiotics and analgesics.
Incision & Drainage: It is drained under regional/general
anaesthesia by placing horizontal/oblique incision parallel to
the palmar crease. Pus is drained and sent for culture and
sensitivity. Thorough saline irrigation is very essential. Drain is placed through the wound.
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7. Ainhum [2000]
Ans.
Ainhum also known as 'dactylolysis spontanea' is a painful constriction of
the base of the 5th toe frequently (occasionally other toes also) followed
by bilateral spontaneous autoamputation a few years later.
 Grooving  pain  constriction deepens  tendon, nerve & vessel involvement  bone gets cut
spontaneously without any bleeding (auto-amputation) in many (2-5) years.
:
 Commonly affects males & Common in blacks, in Negroes.
 History of running barefoot in childhood is common.
 Fifth toe is commonly affected; (Gangrene of little toe). Often it can be bilateral.
: It is early "Z" plasty later amputation. Most often autoamputation occurs.
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1) Madura Foot [21]

Ans.
(MYCETOMA PEDIS) It is a chronic granulomatous condition of the foot
causing multiple discharging sinuses.
Treatment: surgical removal of the lesion followed by use of:
Antifungal agents for eumycetoma (itraconazole or amphotericin B for 8–24 months)
Antibiotics for actinomycetoma, such as Welsh regimen (amikacin plus cotrimoxazole).
1) PET-CT [21]
Ans.
It is a medical imaging technique using a device which combines in a single
gantry system both a PET-scanner & a CT scanner.
Preparation: Fasting for 4-6 h before injection of 18F- FDG
The blue-purple rectangle a represents CT coverage & the overlapping green
rectangle represents PET coverage

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2) Complications of Cyclophosphamide Chemotherapy [19]
Ans.

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3) Sarcoma [08, 06]
Ans.
----------------------------------------------------------------------------------------------------------------------------------------
4) Malignant tumor character and its method of spread [07]
Ans.
FEATURES BENIGN TUMORS MALIGNANT TUMORS (CANCER)
I. CLINICAL AND GROSS FEATURES:
1. BOUNDARIES Well-circumscribed Irregular
2. LOCAL INVASION Often compresses the surrounding tissues Usually infiltrates and invades the adjacent
without invading or infiltrating them tissues
3. METASTASIS Absent Frequently present
4. SECONDARY CHANGES Usually not seen Usually seen
5. NOMENCLATURE They are generally named by attaching the They are termed as carcinoma or sarcoma
suffix “oma” to the cell of origin. {ex: depending on the parenchymal cell of origin.
lipoma} {ex: Liposarcoma & Squamous cell carcinoma}
6. RATE OF GROWTH slow rapid
II. MICROSCOPIC FEATURES
1. PATTERN Well Differentiated (Usually resembles the Poor resemblance to tissue of origin (Anaplasia
tissue of origin closely) is Characteristic)
2. NUCLEO-CYTOPLASMIC Normal Increased
RATIO
3. NUCLEUS Uniform Nuclei Nuclear Pleomorphism & Hyperchromasia
4. INVASION Absent Through basement membrane or into local
tissue
5. MITOTIC ACTIVITY Minimal High with atypical mitosis
6. ANAPLASIA Not seen Can be seen
III. PROGNOSIS Local complications Death by local and metastatic complications
 : Lymphatics, Hematogenous, Spread along body cavities, Direct transplantation, and rarely Along epithelial lining.
Lymphatic Spread: Most common mode of spread for carcinomas. e.g., carcinoma of breast &
carcinoma of lung
Sentinel lymph node: 1st node in a regional lymphatic drainage that receives lymph flow from the
primary tumor. Sentinel lymph node biopsy is done to know the presence or absence of metastatic
lesions.
Skip metastasis: When local lymph nodes are bypassed and lymphatic metastases develop in lymph
nodes distant from the site of the primary tumor; these are called “skip metastasis”. Example:
Virchow’s lymph node is metastasis to supraclavicular lymph node from cancers of abdominal
organs (e.g., Stomach cancer).
Retrograde metastasis: Tumors spreading against the flow of
lymphatics may cause metastases at unusual sites. Example:
Carcinoma prostate metastasizing to supraclavicular lymph node.
Significance of lymph node metastases: Prognostic value, e.g., in
breast cancer, involvement of axillary lymph nodes is very
important for assessing prognosis and for type of therapy.
Hematogenous Spread:
This is common for for sarcomas e.g., angiosarcoma, osteosarcoma etc.
Some carcinomas like renal cell carcinoma & hepatocellular carcinoma also show hematogenous
spread
Cancer metastasizing to bone thyroid, prostate, lung, breast, liver, intestine & kidney.
1. Carcinomas of the thyroid and prostate spread through the paravertebral venous plexus.
2. Radiograph appearance of bone metastasis:
 Osteolytic lesion: radiolucency (e.g., lung
cancer) → pathological fractures and
hypercalcemia.
 Osteoblastic lesion: radiodensities (e.g.,
prostatic cancer, breast, thyroid) and ↑
serum alkaline phosphatase due to reactive
bone formation.
Trans celomic spread:
a) Malignant cells shed from the organ surfaces (e.g., ovaries, GIT, and lung) into the body cavities
b) Body cavities include peritoneal (most common), pleural cavities (common), pericardial
(occasionally), joint space and subarachnoid space.
c) Peritoneal cavity: Example: (1) Ovarian tumors, (2) malignant GIT tumors involve peritoneal cavity
→ ascites.
d) Pleural cavity: Peripherally situated lung tumors → pleural effusions
CSF: Glioblastoma commonly spread through CSF in the subarachnoid space to the spinal cord.
Direct Transplantation of Tumor cells: e.g., by surgical instruments like scalpel, needles,
sutures or implantation by direct contact (e.g., transfer of cancer of lower lip to the corresponding
opposite site in the upper lip).
Spread along the epithelial lined spaces: It is not common. Ex:
 Ca endometrium may spread to ovary (or vice versa) via fallopian tube.
 Ca kidney may spread to lower urinary tract via ureters.
 Drop metastasis: Medulloblastoma invades ventricles & spreads via CSF into spine.
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1. Tumour Markers [21, 13]
Ans.

Tumor markers are products of

malignant tumors that can be
detected in the cells themselves or
in blood and body fluids.

:
Detection of cancer, e.g., PSA is
used to screen prostatic
adenocarcinoma
Determine the effectiveness of
therapy
Detection of recurrence

----------------------------------------------------------------------------------------------------------------------------------------
2. Complications of Radiotherapy [20, 18]
Ans.
Early complications Late complications
Nausea and vomiting – give  Persistent anaemia
anti-emetics  Chronic pelvic pain (due to fibrosis of nerve trunks)
Bladder & rectal irritation –  Post-irradiation ulcers in the bladder  dysuria,
give anti-cholinergics haematuria and vesicovaginal fistula.
Pyelitis, pyelonephritis and  Ureteric stricture and obstructive uropathy
cystitis – give Urinary  Colonic ulcer, perforation, stricture or obstruction
antiseptics and analgesics  Small bowel ulcer, perforation, stricture or obstruction
Malaise, headache and  Cervical stenosis  Pyometra
irritability  Vaginal stenosis  marital discord
Flare-up of sepsis, pyometra &  Disturbed psyche
peritonitis  Ovarian destruction  menopausal symptoms 
Skin reaction osteoporosis  fracture neck of the femur
Pulmonary embolism  Sarcoma
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3. Lupus Vulgaris [20]
Ans.
: It is cutaneous tuberculosis which occurs in young age group.
: Commonly seen on face, hand and forearm;
:
 It starts as typical apple-jelly nodule with congestion of skin around.
 Glass slide pressed firmly on the diseased area to eliminate the surrounding
hyperaemia causes clinically obvious apple-jelly appearance
 Eventually a superficial ulcer with undermined edge is formed.
 The ulcer is active with destruction occurs at the periphery and healing taking place at the centre.
Often lesion extends into nose and oral cavity involving the mucosa.
: Due to lymphatic obstruction facial oedema can occur. Long-standing lupus vulgaris
can turn into squamous cell carcinoma
: ESR, discharge study, biopsy, chest X-ray.
: Anti-tuberculous drugs  If complete healing does not occur  excision and skin grafting
----------------------------------------------------------------------------------------------------------------------------------------
4. Grading and staging of malignant tumours [06]
Ans.
Grading and staging gives information about the aggressiveness of tumors and their extent & spread in
individual patients. Low-grade tumors are well-differentiated; high-grade ones tend to be anaplastic.
Significance:
1) To determine the treatment protocols &
2) To predict the prognosis of tumor
Grading: It is based on the degree of differentiation and no. of mitoses of the tumor. Range from 2 to 4
categories
Staging: It is based on the size of primary tumor, its extent of spread to regional lymph nodes, and the
presence or absence of blood-borne metastases

refers to the size of the primary tumor: T0 for in situ lesion & T1 to T4 on the basis of size of tumor.
refers to lymph node status: N0 for no LN involvement. N1 to N3 on the basis of no. of LNs
involved.
refers to the presence of distant metastases: M0 signifies no distant metastases, whereas M1
indicates the presence of metastases.
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5. Acoustic Neuroma [03]
Ans.
1) Malignant Melanoma – Etiology, C/F, Dx & Mx [10]
a. Breslow's staging [08]
Ans.
Malignant neoplasm of melanocytes
Sites: Skin (MC) – Upper back in men; Back & legs in women
Others: Esophagus; mucous surfaces of oral & anogenital tracts
Risk factors: Fair skin (Albinism); Sun exposure (UV
radiation); XP & Dysplastic Nevus
Etiology: Sporadic (MC) or genetic
Pathogenesis: Ultraviolet radiation causes DNA damage
Genetic alterations: 1) Mutations of the gene CDKN2A 2) Activating mutations in BRAF 3)
Mutations activating telomerase enzyme
Gross: Mole-like growth with “ABCD”
 Asymmetry; Borders are irregular; Color is not uniform; Diameter > 6 mm
 Patterns of growth:
1. Radial growth: Horizontal spread within the epidermis & superficial dermis. No metastatic risk.
2. Vertical growth: Invasion into dermis is seen with appearance of a nodule. ↑ risk of Metastatic.
Histopath.: Melanoma cells are seen with large nuclei having peripheral chromatin clumping & red
nucleoli.
C/P: Asymptomatic; Itching or pain may be seen.
Prognosis: Favorable prognosis is with female gender, thinner tumor depth (Breslow thickness),
few mitoses, lack of ulceration & absence of lymph node metastasis.
Metastasis: Regional lymph nodes {Dx is made by FNAC}
Management – Surgery is the main treatment
 Treatment options for primary:
 Handley's wide local excision (WLE)
 If primary area is wide and deep, then amputation with one joint above is done
 In fingers and toes, disarticulation is required
 Melanoma in anal canal may require abdominoperineal resection.
 Enucleation in case of melanoma in eye
 Melanoma in pregnancy is treated with termination of pregnancy and specific therapy for
melanoma
 Treatment options for lymph node secondaries – Chemotherapy for fixed LN {since it is inoperable}
 Drugs used – (Diethyl triamine iminocarboxamide); CVD regime
----------------------------------------------------------------------------------------------------------------------------------------

1. Basal cell carcinoma / Rodent Ulcer [21, 17, 11, 03]

a. Treatment of Malignant Ulcer Cheek [03]
Ans. It is a low grade, locally invasive, carcinoma arising from basal layer of skin or mucocutaneous
junction. It does NOT arise from mucosa.
 Risk factors: Sun (UV) exposure; Males, Old age; White-skin; Albinism; Xeroderma pigmentosum;
Immunosuppression; Exposure to arsenics, coal tar, aromatic hydrocarbons etc.
It is the commonest malignant skin tumour.
Sites involved:
 MC is along the Ohngren's line in Face.
 It is called as tear cancer because it is commonly seen in
area where tears roll down.
Etiopathogenesis: Sporadic or genetic.
• Loss of function mutations in PTCH gene, that activate the
Hedgehog signaling pathway
• BCC is Locally aggressive, slow-growing & rarely metastasize
• Types of BCC:
Morphological Types of BCC Clinicopathological Types of BCC
- Nodular (MC);
a. Superficial type – small buds of tumour
- Cystic/nodulocystic;
masses, common in young people.
- Ulcerative – Rodent (Jacob) ulcer;
b. Morpheic type – dense stroma with
- Pigmented BCC – mimics melanoma.
basal cells and type IV collagen; spreads
- Geographical or Field Fire or Forest Fire BCC
rapidly; sclerosing BCC.
- Basisquamous – behaves like squamous cell
carcinoma which spread into lymph nodes. BCC which has c. Fibroepithelioma type – seen on lower
not been treated for long time can turn into Basisquamous back.
carcinoma
• Metastasis: It does not spread through lymphatics nor through the blood. But it erodes deeply
into local tissues including cartilages, bones causing extensive local destruction. Hence the
name "Rodent ulcer".
 Clinical Presentation: Ulcer on the face in a middle-aged man which is nontender, dry, slowly
growing, nonmobile, with raised and beaded edge with central scab
 Site of beading signifies the area of active proliferating cells
 Histological Appearance:
1. Cords of basophilic cells with hyperchromatic  Size >2 cm  Recurrent tumours
 Near the  Immunosuppressed
nuclei, surrounded by lymphocytes & fibroblasts. eye/nose/ear
2. Basaloid Cells exhibit peripheral palisading  Ill-defined margins
3. Stroma is seen retracting away from tumor creating artifacts.
DDx: Squamous cell carcinoma; Melanoma; Keratoacanthoma; Seborrhoeic keratosis.
Investigations: Wedge biopsy, X-ray of the part, CT scan dermoscopy is very useful
Treatment:
 Curative Radiotherapy – since BCC is radiosensitive.
 Indications for Surgery: Radiotherapy is NOT given, once BCC erodes into cartilage or bone, BCC
arising near ear, eye & in Recurrent BCC. In such cases, Surgery us preferred.
 Surgical Options:
1. Wide excision (4-6 mm clearance) with skin grafting, primary suturing or flap (Z plasty,
rhomboid flap, rotation flap) is the procedure of choice.
2. Cryosurgery
3. MOHS (Microscopically Oriented Histographic Surgery)
4. Other options: Laser surgery, photodynamic therapy, curettage and electrodesiccation etc.
Associations of BCC: Nevoid basal cell carcinoma syndrome or Gorlin syndrome
----------------------------------------------------------------------------------------------------------------------------------------
2. Squamous Cell Carcinoma [19, 05, 04]
a. Epithelioma [15, 12]
Ans.
Premalignant conditions of SCC: Bowen's disease, Paget's disease, leukoplakia, chronic scars,
chemically induced chronic irritation, radiodermatitis, senile keratosis
Sites: Dorsum of hand, limbs, face, and skin of abdominal wall, external genitalia, mucocutaneous
junction, oral cavity, respiratory system, oesophagus, gallbladder, in urinary bladder as metaplasia
from transitional cell lining.
Risk Factors: Males; Exposure to UV B rays, mutation of p53 suppressor gene (seen in 90% SCC).
An ulcero-proliferative with Raised and everted edge; indurated base; Bloody
discharge from the lesion. Regional lymph nodes are commonly involved
Marjolin’s ulcer, Verrucous carcinoma
: BCC; Melanoma; Keratoacanthoma; Skin adnexal tumours; Actinic keratosis;
Pyogenic granuloma.

 Wedge biopsy from the edge.

 FNAC from lymph node.
 CT scan to identify nodal disease;
 MRI to identify local extension is useful.

 Radiotherapy
 Wide excision, 2 cm clearance followed by skin grafting or flaps.
 Amputation with one joint above.
 For lymph nodes, block dissection of the regional lymph nodes is done.
 Chemotherapy is given using methotrexate, vincristine, bleomycin, cisplatin, carboplatin.
 Field therapy using cryo probe or topical fluorouracil or electrodessication.
1. Skin grafting [11, 01]
a. Autograft [11]
b. Thiersch Graft [08]
c. Free Skin Graft [05]
Ans.
 Skin Grafting refers to the transfer of skin from one area
(donor area) to the required defective area (recipient
area).
 It is an autograft.
 Types of Skin Graft:
Partial thickness graft Full thickness graft
 – aka Split-thickness skin graft – SSG & Thiersch graft  – aka Wolfe Graft
 It is removal of full epidermis + part of the dermis from the  It includes both epidermis+
donor area full dermis
 Depending on the amount of thickness of dermis taken, it can  It is used over the face,
be (1) Thin SSG; (2) Intermediate SSG; (3) Thick SSG eyelid, hands, fingers and
 Donor area – thigh (MC), occasionally arm, leg, forearm over the joints
 Advantages: technically easy; can be used to cover large defect  : No
 Disadvantages: Contractures will form contracture
GENERAL SURGERY
PAPER – 1
ORTHOPAEDICS

SMAHRT NOTES
ORTHOPAEDICS ...........................................................................................................................................5
Anatomy of Bone & Fracture Healing ........................................................................................................5
...........................................................................................................................................................5

...........................................................................................................................................................6

.........................................................................................................................................................6
Recent Advances in Treatment of Fracture ...............................................................................................8
...........................................................................................................................................................8

.........................................................................................................................................................8
Splints & traction ......................................................................................................................................10
.........................................................................................................................................................10
Complications of Fracture ........................................................................................................................12
.........................................................................................................................................................12

.......................................................................................................................................................16
Peripheral Nerve Injury ............................................................................................................................17
.........................................................................................................................................................17

.......................................................................................................................................................20
Injuries around Shoulder Joint .................................................................................................................22
.........................................................................................................................................................22

.........................................................................................................................................................23
Injuries around Elbow Joint......................................................................................................................26
.........................................................................................................................................................26

.........................................................................................................................................................27

.......................................................................................................................................................27
Injuries to Forearm & Wrist .....................................................................................................................29
.........................................................................................................................................................29

.........................................................................................................................................................30

.......................................................................................................................................................30
Hand Injuries .............................................................................................................................................31
.........................................................................................................................................................31
 .......................................................................................................................................................31
Pelvic Fractures .........................................................................................................................................32
.........................................................................................................................................................32
Injuries around Hip ...................................................................................................................................33
.........................................................................................................................................................33

.........................................................................................................................................................34
Fracture Shaft of Femur............................................................................................................................36
.........................................................................................................................................................36

.........................................................................................................................................................36
Injuries around Knee joint ........................................................................................................................37
.........................................................................................................................................................37

.......................................................................................................................................................39
Injuries to Leg, Ankle & Foot ....................................................................................................................41
.........................................................................................................................................................41

.........................................................................................................................................................42

.......................................................................................................................................................42
Infections of Bone & Joint ........................................................................................................................43
.........................................................................................................................................................43

.........................................................................................................................................................45

.......................................................................................................................................................46
TB of Bone & Joints ...................................................................................................................................47
.........................................................................................................................................................47

.........................................................................................................................................................48

.......................................................................................................................................................49
Congenital Talipes Equino Varus ..............................................................................................................50
.........................................................................................................................................................50
Congenital Dislocation of Hip ...................................................................................................................52
.........................................................................................................................................................52

.........................................................................................................................................................52

.......................................................................................................................................................54
Neuromuscular Disorders.........................................................................................................................55
 .........................................................................................................................................................55

.......................................................................................................................................................55
Bone Tumors .............................................................................................................................................56
.........................................................................................................................................................56

.........................................................................................................................................................57

.......................................................................................................................................................60
Metabolic Bone Disease ...........................................................................................................................61
.........................................................................................................................................................61

.......................................................................................................................................................63
Amputation & Prosthetics ........................................................................................................................64
.........................................................................................................................................................64

.......................................................................................................................................................64
Prolapsed Intervertebral Disc ..................................................................................................................65
.........................................................................................................................................................65

.........................................................................................................................................................66
Spinal Injuries............................................................................................................................................67
.........................................................................................................................................................67

.........................................................................................................................................................67
Arthritis & Related Disorders ...................................................................................................................69
.........................................................................................................................................................69
Degenerative Disorders ............................................................................................................................72
.........................................................................................................................................................72

.........................................................................................................................................................72

.......................................................................................................................................................73
Affections of Soft Tissue ...........................................................................................................................74
.........................................................................................................................................................74

.......................................................................................................................................................74
Miscellaneous ...........................................................................................................................................76
.........................................................................................................................................................76

.......................................................................................................................................................78
 ORTHOPAEDICS
Anatomy of Bone & Fracture Healing

1. Define fracture and describe bone healing [10]

a. Healing of fracture [16]
b. Pathology of fracture healing, factors influencing it and complications of fractures [04]
Ans.
A fracture is defined as a break in the continuity of a bone.
Healing of Fractures: Fracture healing involves reactivating bone formation pathways, regulated by
cytokines and growth factors.
Events & Stages: �
During the first week
 Hematoma forms immediately after fracture, filling the fracture gap
 Clot provides a fibrin meshwork for the influx of inflammatory cells and
ingrowth of fibroblasts and new capillaries
 Growth factors (PDGF, TGF-γ & FGF) activate osteoprogenitor cells and
stimulate osteoclastic and osteoblastic activity
 Finally, uncalcified tissue called, soft tissue callus is formed providing
anchorage between the ends of fractured bones.
Within 2 weeks
 Activated osteoprogenitor cells deposit subperiosteal trabeculae
 Activated mesenchymal cells differentiate into chondrocytes to make cartilage
which undergoes endochondral ossification
 Finally, soft tissue callus is transformed into a bony callus which stabilizes the
fracture site.
 Bony callus is eventually
remodeled along lines of
weight bearing and the
healing process is complete
with lamellar bone having
medullary cavity.
Factors that influence healing:
Inadequate immobilization,
malalignment, infection of the
fracture site, malnutrition and
skeletal dysplasia
Complications: Delayed union or nonunion; Pseudoarthrosis
----------------------------------------------------------------------------------------------------------------------------------------
1) Pathological fractures [17, 13, 11, 06, 02]
Ans.
A Fracture is termed pathological when it occurs in a bone
made weak by some disease
Causes
 A bone may be rendered weak by a disease localised to
that particular bone, or by a generalised bone disorder.
 Osteoporosis is the MCC of pathological fracture
Diagnosis: pain in the affected bone BEFORE the fracture.
Treatment:
 Detect the underlying cause of the fracture; and
 Make an assessment of the capacity of the fracture to unite,
based on the nature of the underlying disease. Ex:
 Fracture at the site of a bone cyst or a benign tumour will
generally unite, but the union may be delayed
 Fractures in osteomyelitic bones often take a long time to
unite
 Fractures through metastatic bone lesions often do not
unite at all
 With internal Fixation, enhance the process of union by bone
grafting (e.g., in bone cyst or benign tumour)

----------------------------------------------------------------------------------------------------------------------------------------

1. Types of fractures [20, 18]

a. Classification of open fractures [19]
Ans.
Types of fractures
On the Basis of
1. Traumatic fracture
Etiology 2. Pathological fracture
3. Stress Fracture
a) Undisplaced fracture
Displacements
b) Displaced fracture
A. Closed fracture – does NOT communicate with External Environment
B. Open fracture – communicate with External Environment due to break in
Relationship with the overlying skin or soft tissues
external Classification of Open fractures:
environment 1. Internally open (from within) – sharp fracture end pierces the skin from within
2. Externally open (open from outside): External object lacerates the skin and soft
tissues over the bone & then breaks the bone
Complexity of a. Simple fracture: A fracture in two pieces – easy to treat – Ex: a transverse
treatment fracture of humerus
 b. Complex fracture: A fracture in multiple pieces – difficult to treat – Ex: a
comminuted fracture of tibia
1) High-velocity injury - # due to severe trauma as in RTA – a/w severe soft
Quantum of force tissue injury.
causing fracture 2) Low-velocity injury - # due to mild trauma force as in fall - little soft tissue
injury
Transverse fracture – # line is ⊥ar to the long axis of the bone
Oblique fracture - # line is oblique
Spiral fracture - # line runs spirally
in more than 1 plane
Pattern
Comminuted fracture – it is a #
with multiple fragments.
Segmental fracture – there are 2 #
in one bone, but at different levels.
----------------------------------------------------------------------------------------------------------------------------------------
2. Stress fracture [09]
Ans.
 This is a special type of # sustained due to chronic repetitive injury (stress)  break in bony trabeculae.
 Clinical Presentation: These often present as only pain and may not be visible on X-rays.
 Best diagnostic test for unilateral stress fracture is MRI, and for bilateral is bone scan
 Example: March fracture is a type of stress fracture of shaft of 2nd metatarsal
 Recent Advances in Treatment of Fracture

1) Internal fixation of recent fractures [08]

Ans.
Internal fixation is an operative method for immobilisation of #
In this method, the fracture, once reduced, is held internally with the help of an implant which are
made of high quality stainless steel to which the body is inert.
:
When a fracture is so unstable that it is difficult to maintain it by nonoperative means.
As a treatment of choice in some fractures, in order to secure rigid immobilisation and to allow
early mobility of the patient.
When it has been necessary to perform open reduction for reasons such as an associated
neurovascular injury.
: A fracture can be fixed internally by any one or combination of implants – Ex: Steel wire,
Kirschner wire, Intra-medullary nail, Plate and screws etc.
 Fracture specific implant – Ex: Talwalkar's nail for # of forearm bones
:
 Minimal need for external immobilisation.
 Early mobility of the patient
 Joints do not get stiff and the muscle functions remain good.
 Complications associated with confinement of a patient to bed are also avoided.
: Infection & non-union.
----------------------------------------------------------------------------------------------------------------------------------------
2) Methods of immobilization [06]
Ans.
Immobilisation of a fracture can be done by non-operative or operative methods.
– Ex: Strapping, sling, cast, Functional bracing etc.
: Internal fixation & External fixation
----------------------------------------------------------------------------------------------------------------------------------------

1) Allogenous bone grafting [18]

Ans.
 Allogenous bone grafts (Allografts) are needed when enough bone is not available from the host
e.g., where a big defect is created following a tumour resection.
 Such bone grafts could be obtained from another human being, living or dead {cadaveric graft}.
 Allogenous graft from live donors – Ex: from the mother when larger amount of bone graft is
required for a child.
 : Deep freezing (at –70° C), freeze dried, preservation by
decalcifying bone (decal bone), or by formalin preservation.
 Hospitals performing tumour excision surgery in a big way have a regular department procuring
bones from patients and cadavers, processing it and storing it. These are called bone banks.
----------------------------------------------------------------------------------------------------------------------------------------
2) Plaster of Paris [10, 06]
Ans.
This is the most common method of immobilisation of #.
Plaster of Paris (Gypsum salt) is CaSO4 ½ H2O in dry form
Minerva cast for Cervical spine disease; Colle’s’ cast for Colle’s’ #.
Plaster of Paris can be applied in 2 forms i.e., slab or a cast.
:
 Immobilise the joints above and below the fracture.
 Immobilise joints in a functional position
 Pad the limb adequately, especially on bony prominences
: avoid wetting, notice for any cracks etc.
: Impairment of circulation (tight cast) & Plaster sores
 Splints & traction

1. Thomas splint [13, 10, 09, 07]

Ans.
It is one of the commonest splints used in orthopaedic practice. It was devised by H.O. Thomas,
initially for immobilisation for TB of the knee.
Parts of a Thomas splint:
 It has a ring and two side bars joined distally.
 The ring is at an angle of 120° to the inside
bar.
 The outside bar has a curvature near its
junction with the ring to accommodate the greater trochanter.
Size of a Thomas splint: This is measured by finding the ring size and the length of the splint.
• Ring size = 2 inches + thigh circumference at the highest point of the groin.
• Length of a Thomas splint = 6 inches + Length of the highest point on the medial side of the
groin up to the heel.
Uses: A Thomas splint is used for immobilisation of the lower limb.
 The ring of the Thomas splint is introduced around the limb.
 The thigh and leg are supported on slings tied over the side bars
----------------------------------------------------------------------------------------------------------------------------------------
2. Objectives & Types of Tractions [21, 17, 13]
a. Skeletal traction [11]
b. Skin traction [96]
Ans.
Traction is the practice of pulling on a broken bone or dislocated body part in a slow, steady manner to
realign it into proper position and keep it stable. This is typically done with ropes, weights, and pulleys

Objectives of Traction: Traction is used for:

1) Reduction of fractures and dislocations, and their maintenance;
2) For immobilising a painful, inflamed joint;
3) For the prevention of deformity, by counteracting the muscle spasms associated with painful
joint conditions; and
4) For the correction of soft tissue contractures by stretching them out.

Types of Tractions: For effectiveness of any traction, a counter-traction is necessary. Depending

upon what acts as countertraction, a traction can be fixed or sliding.
Fixed traction Sliding traction
In this type, counter-traction is provided by a In this type, the weight of the body acts as
part of the body counter-traction
Ex: In Thomas splint fixed traction, the ring of Ex: In traction given for a pelvic fracture the
the splint comes to lie against the ischial foot-end of the bed is raised so that the weight
tuberosity and provides counter-traction of the body acts as counter-traction
 Methods of applying traction: There are 2 methods of applying traction – skin and skeletal
Skin traction Skeletal traction
An adhesive strap is applied on the skin. The
The traction is applied directly on
traction force is transmitted from the skin
Method the bone by inserting a K-wire or
through the deep fascia and intermuscular
Steinmann pin through the bone
septae to the bone
Required for Mild to moderate force Moderate to severe force
Used in Children Adults
Duration Short Long
Common site Below knee Upper tibial pin traction
 Complications of Fracture

1) Myositis ossificans [16, 2000]

Ans.
It is aka post-traumatic ossification.
Causes:
 In severe injury to a joint, the capsule and the periosteum will be stripped from the bones by
violent displacement of the fragments.
 At High-Risk: Children (loos periosteum), injury at elbow joint, head injury (neuronal damage),
paraplegics & Massage following injury.
Pathogenesis: severe injury to a joint  haematoma formation around the joint  ossification of
the haematoma  formation of a mass of bone  joint movements restricted
Consequences:
 The bone formation leads to stiffness of the joint.
 In extreme cases, the bone bridges the joint resulting in complete loss of movements (extra-
articular ankylosis).
 Radiologically, an active myositis (margins of bone mass are fluffy) and a mature myositis
(margins are well-defined) have been identified.
Treatment:
 Massage following injury is strictly prohibited.
 In the early active stage of myositis, give rest to the limb & start NSAIDs.
 In late stages, physiotherapy help to regain movement.
 In cases of mature myositis, surgical excision of the bone mass may help regain movement.
----------------------------------------------------------------------------------------------------------------------------------------
2) Compartment Syndrome [19, 14, 09]
Ans.
Compartment syndrome is a condition in which a rise in pressure
within a limb’s anatomical compartments jeopardize the blood
supply to the muscles and nerves within the compartment
Causes:
The rise in compartment pressure can be due to:
 Any injury leading to oedema of muscles.
 Fracture haematoma within the
compartment.
 Ischaemia to the compartment, leading to
muscle oedema.
High index of suspicion – Excessive pain at
injury, not relieved with usual doses of
analgesics
Injuries with a high risk of developing
compartment syndrome are:
 Supracondylar fracture of the humerus
 Forearm bone fractures
  Crush injuries to leg and forearm
 Closed tibial fractures
Consequences:
  pressure within the compartment compromises the circulation  further muscle ischaemia  A
vicious cycle is thus initiated (Eaton & Green Cycle)  ischaemic muscle necrosis, nerve damage.
Gangrene can occur in severe cases
 The necrotic muscles heal with fibrosis contractures
 Nerve Damage  motor and sensory loss
Diagnosis:
: The ischaemic muscles, when stretched, give rise to pain – This is the earliest sign of
impending compartment syndrome
Other signs include a tense compartment, hypoesthesia in the distribution of involved nerves,
muscle weakness etc.
– measure compartment pressure. A pressure higher than 40 mm of water is
indicative of compartment syndrome (palpation of pulses is NOT reliable!!!).
Treatment:
 Preventive measures: Limb elevation, active finger movements, close watch for early signs etc.
 Surgical decompression is necessary in established cases. This can be done by:
 Fasciotomy: The deep fascia of the compartment is slit longitudinally (e.g., in forearm).
 Fibulectomy: The middle 3rd of the fibula is excised to decompress all compart­ments of the leg.
----------------------------------------------------------------------------------------------------------------------------------------
3) Non-Union [09, 06, 03]
Ans.
It refers to those fractures which fail to unite even after 6
months
:�
:
 Persistent pain, deformity, or abnormal mobility at the
fracture site
 Non-union may be painless if pseudo joint forms between the
fracture ends (pseudoarthrosis).
 Common sites for non-union: neck of the femur, scaphoid,
lower third of the tibia, lower third of the ulna and lateral
condyle of the humerus
:
 Made clinically using serial X-rays in relation to time.
 X-rays fail to show bony union
 X-ray findings: The fracture line is visible with a little bridging
callus. The fracture ends can be rounded, smooth and
sclerotic & the medullary cavity may be obliterated
 Stress X-rays or weight bearing X-rays can be used to
demonstrate mobility at the fracture by.
 3-D CT scan is helpful in differentiating between delayed and
non-union
 of non-union depends upon the site and the disability caused by it:
No treatment – if patient is asymptomatic – Ex: some non-unions of the fracture scaphoid
Open reduction, internal fixation and bone grafting {grafts are taken from iliac crest}
Excision of fragments – done where the excision will not cause any loss of functions. It can be
combined with replacement with an artificial mould (prosthesis).
Ex: In non-union of fracture of the neck of femur in an elderly, the head of the femur can be
replaced by a prosthesis (replacement arthroplasty).
Ilizarov’s method – external fixation apparatus for treating non-union
----------------------------------------------------------------------------------------------------------------------------------------
4) Volkmann's ischaemic contracture [08, 07, 05, 03]
a. C/F of Volkmann's ischaemic contracture [14]
Ans.
VIC is a late complication of Supracondylar Fracture of the Humerus.
: This is a sequel of Volkmann’s ischaemia  ischaemic muscles are gradually replaced by
fibrous tissue, which contracts and draws the wrist and
fingers into flexion �
:
There is marked atrophy of the forearm, with flexion
deformity of the wrist and fingers.
Skin over the forearm and hand is dry and scaly. The nails
also show atrophic changes.
Volkmann’s sign –fingers extend fully at the
interphalangeal joints only when the wrist is flexed. On
extending the wrist, the fingers get flexed at the inter-phalangeal joints. This is because when the wrist
is extended, the shortened flexor muscle-tendon unit is stretched over the front of the wrist  flexion of the fingers.
If the peripheral nerves are also affected, there will be sensory loss and motor paralysis in the
forearm and hand
:
by passive stretching of the contracted muscles, using a turn-buckle splint
(Volkmann’s splint).
- Maxpage operation – flexor muscles are released from their origin at
the medial epicondyle and ulna.
, bone operations such as shortening of the forearm bones, carpal bone
excision etc. may be required
----------------------------------------------------------------------------------------------------------------------------------------
5) Complications of a fracture [08]
a. Malunion of fracture [21, 20, 06]
Ans.
Complications of fractures can be classified into three broad groups depending upon their time of
occurrence:
a) Immediate complications – occurring at the time of the fracture
b) Early complications – occurring in the initial few days after the fracture.
c) Late complications – occurring a long time after the fracture.
 : When a fracture does not unite in proper
position which leads to a significant disability, it is said to
have malunited.
:
Improper treatment - MCC.
Sometimes, malunion is inevitable because of unchecked
muscle pull (e.g., fracture of the clavicle), or excessive
comminution (e.g., Colle’s’ fracture).
:
Deformity, shortening of the limb & limitation of
movements.
Common sites: Fractures at the ends of a bone always
unite, but they often malunite e.g., supracondylar
fracture of the humerus, Colles’ fracture etc.
: Significant malunion (with disability) needs
operative intervention. The options are:
Osteoclasis (refracturing the bone) – Under GA, fracture is
recreated, the angulation corrected, and the limb
immo­bilised in plaster.
Redoing the fracture surgically – The fracture site is
exposed, the malunion corrected and the fracture fixed internally with suitable implants.
Corrective osteotomy – in cases of poor skin condition, poor vascularity of bone in that area etc.,
the deformity is corrected by osteotomy at a site away from the fracture as the healing may be
quicker at this new site, e.g., supra-malleolar corrective osteotomy for malunion of distal-third
tibial fractures.
Excision of the protruding bone – Ex: In a fracture of the clavicle, a bone spike protruding under
the skin may be shaved off.
Sometimes malunion may not need any treatment because it is expected to correct by
remodelling – Ex: in Children
----------------------------------------------------------------------------------------------------------------------------------------
6) Osteitis deformers [07]
a. Paget’s Disease of Bone [04, 02]
Ans.
Paget’s Disease of Bone {Osteitis deformans} is a condition characterised by a progressive tendency
for one or more bones to bend, get thickened and spongy.
– Idiopathic; mostly triggered by infections like measles etc.
Due to defect in the osteoclast   irregular bone resorption & bone turnover
: Tibia is most commonly affected – the bone is soft in the initial stages, but becomes dense
and hard later.
: The disease begins after 40 years of age.
 Initial stages – asymptomatic
In late stages – misshapen bones can:
 Impinge on nerves  pain; dull in nature
 Impinge on optic nerve  vision loss
 Overgrow  leontiasis (lion facies);
 Narrow auditory foramen  hearing loss
 Kyphosis, pelvic asymmetry & lower limb
weakness etc.
:
 X-rays show multiple confluent lytic areas with interspersed new bone formation.
 Bone scan shows an increased uptake.
 Serum alkaline phosphatase is elevated.
pathological fracture; Osteosarcoma.
is by calcitonin or bisphosphonate.
----------------------------------------------------------------------------------------------------------------------------------------

1. Greenstick fracture [13]

Ans.
It refers to fracture in children where the outer cortex breaks and the inner cortex bends
Cause: Bones in children are more resilient and springier, withstanding greater
deformation without complete fracture
Occurs only in children
Such fractures occur commonly in the shafts of forearm bones
 Peripheral Nerve Injury

1) Foot drop [21, 09, 08, 04]

Ans.
Definition: Inability to actively dorsiflex and evert the foot
Etiology: It occurs in common peroneal nerve palsy �.
 Traumatic causes: injuries to dorsiflexors of foot {can be direct
or iatrogenic}
 Infective causes – leprosy, Poliomyelitis, Syphilis etc.
 Metabolic – DM, Beri Beri etc.
 Exogenous toxin – Lead, Arsenic, Mercury etc.
Clinical Features:
Difficulty in lifting the foot;
Dragging the foot on the floor as one walks
Characteristic “High Stepping Gait” {Ball of Foot instead of heel hits the ground}
Pain, weakness or numbness in the foot
Signs:
Cutaneous sensation is impaired over the lateral aspect of the lower leg and ankle and dorsum
of the foot
Reduced dorsiflexion and eversion of the foot and of toe extension {Inversion & plantar flexion are normal}
The paresis results in ankle weakness and predispose to ankle sprains
Diagnosis
X-ray – for post-traumatic cases – Anatomic dysfunction (e.g. Charcot joint)
Ultrasonography – If bleeding is suspected in a patient with a hip or knee prosthesis
Magnetic Resonance Neurography – Tumor or a compressive mass lesion to the peroneal nerve.
Electromyelogram – to confirm the type of neuropathy, establish the site of the lesion, estimate
extent of injury, and provide a prognosis.
Treatment
Treat the underlying cause
Medical treatment – for painful paresthesias – amitriptyline, nortriptyline & pregabalin
Assistive devices – to help in walking – Ex: Canes, crutches, or walkers
Electrical Stimulation – Ex: Transcutaneous electrical nerve stimulation (TENS) to  pain.
Protective Devices – Ex: splints, orthoses – splint knee in 20° of flexion & ankle in 90° for night
time
Cryotherapy, massage
Surgery – done if conservative management fails;
 Principles of various surgeries: Repairs or decompression of a damaged nerve, fusion of the
foot and ankle joint or transfers tendons from stronger leg muscles
 Tendon Transfer Surgeries – Ex: Barr’s Technique (anterior transfer of tibialis posterior).
----------------------------------------------------------------------------------------------------------------------------------------
2) Claw hand [21, 11, 05, 04]
a. Ulnar claw hand [15]
Ans.
: Claw hand is an abnormal hand position that develops due to a problem
with the ulnar nerve or, Both ulna and median nerve
: Claw hand means hyperextension at the metacarpo-
phalangeal joints and flexion at the proximal and distal inter-phalangeal joints
: paralysis of the lumbricals {they flex the metacarpo-phalangeal joints and extend the inter-phalangeal joints}.
Leprosy is the MCC
Also seen in congenital defect, wrist injury;
Risk factors: older males; cyclist, desk jobs, elbow leaning, string musicians etc.
:
– Involve only ulnar 2 digits {medial two fingers} – seen in isolated ulnar nerve palsy
– All the 4 fingers develop clawing in combined median & ulnar nerve palsies.
:
Typical Position of Deformity
Loss of abduction/adduction of the fingers – difficulty in turning doorknobs, keys inlock etc.
Wartenberg’s sign – Little finger remains permanently abducted from the ring finger
Numbness in the distribution of involved nerves
Median nerve thenar muscle paralysis  Simian palm deformity – thumb metacarpal moves
dorsally into the plane of the finger metacarpals due to the unopposed extension of the pollicis
longus tendon
– Volkmann’s Contracture; Dupuytren’s Contracture; Spastic Hand; Peripheral neuropathies
– Nerve repair or decompression is the treatment of choice.
If the nerves are unrepairable or repairs have failed, tendon transfer can be considered
----------------------------------------------------------------------------------------------------------------------------------------
3) Tardy ulnar nerve palsy [13]
Ans.
It is a Late complication of Fracture of the Lateral Condyle of the Humerus
: Diminished growth at the lateral side of distal humerus epiphysis 
cubitus valgus deformity (carrying angle) late ulnar nerve palsy (tardy ulnar
nerve palsy) because of friction neuritis of the ulnar nerve as it moves over the medial epicondyle,
every time the elbow is flexed and extended.
– tingling and numbness in the distribution of the ulnar nerve
:
No treatment is required for a mild deformity.
For moderate to severe cases  supracondylar osteotomy to correct the deformity.
Prophylaxis – Anterior transposition of ulnar nerve- the nerve should be transposed anteriorly from
behind the medial epicondyle to prevent friction.
----------------------------------------------------------------------------------------------------------------------------------------
4) Wrist drop [12, 07, 06, 05]
a. Radial nerve injury [13]
Ans.
Wrist drop is a pathological condition in which there is injury to radial nerve resulting in impairment of
nerve function due to which the patient cannot extend their wrist and it hangs flaccidly {wrist drop}.
 :
 Saturday night palsy – {alcoholperson falls asleep with back of
their arm compressed by a chair, bar edge etc.}
 Crutch palsy – compression of nerve from walking with crutch
 Honeymoon palsy – compression of nerve from an individual
sleeping on one’s arm overnight
Radial nerve mainly supplies – Posterior arm & Forearm
– Trauma {penetrating trauma, compressions},
Infection & Exposure to toxins {Ex: lead}
Wrist drop can occur due to UMN lesion or LMN lesion
: The wrist remains in palmar
flexion due to weakness of the dorsiflexors.
are dependent on the site of the lesion:
 Above elbow – numbness in forearm + hand
 In the forearm – wrist drop only (no paraesthesia)
 In the wrist – sensory changes & paresthesias only in back of hand (no motor weakness)

 ROM of wrist – to check for weakness or loss of muscle tone

 CT scan and MRI; Electromyography; Nerve conduction test
: treat the underlying cause
 Analgesic for the pain
 Steroid injections – to inflammation
 Splints, braces, massage, physiotherapy etc.
----------------------------------------------------------------------------------------------------------------------------------------
5) Brachial Plexus Injury [11]
a. Erb's Palsy [03]
b. Klumpke’s' paralysis [01]
Ans.
Brachial Plexus is a major source of motor and sensory supply to the shoulder girdle, the Upper
trunk and the whole of Upper limb.
The brachial plexus is a somatic nerve plexus formed by intercommunications among the ventral
rami (roots) of the lower 4 cervical nerves (C5-C8) and the first thoracic nerve (T1).
:
Brachial Plexus Injury can be due to avulsion, rupture, neuroma or neuropraxia of the nerve
: Shoulder dystocia, Maternal diabetes, macrosomia, Breech presentation at birth,
Motor cycle accidents, Stab and bullet wounds etc.
:
Traction: direct blow to the shoulder with the neck laterally flexed toward the unaffected
shoulder (gymnast falls on beam)
Direct trauma: direct blow to the supraclavicular fossa over Erb's point
Compression: Occurs when the I neck is flexed laterally toward the patient's affected shoulder,
compressing/ Irritating the nerves
:
Upper plexus palsy (Erb's palsy) Involves C5-C6 + C7roots.
 involves C8-T1 roots (and sometimes also C7)
Total plexus lesions Involve all nerve roots C5-T1
–
 Weakness or numbness; Pain; Loss of sensation;
Paralysis
 Deformity in Erb’s Palsy – Policeman’s tip hand
 Complete Claw
Hand

– X-ray of cervical spine, Chest X-ray,

CT scan, MRI & Electromyography

– Conservative & Surgical �

----------------------------------------------------------------------------------------------------------------------------------------

1. Sciatic nerve injury [21]

Ans.
Sciatic nerve consists of 2 – the tibial and common peroneal nerves
The common peroneal component is more frequently affected than the tibial.
Tests: The common peroneal nerve supplies the extensors and the evertors of the foot. The tibial
nerve supplies the plantar flexors of the foot.
Deformity – Foot Drop {Refer 1st SQ}
----------------------------------------------------------------------------------------------------------------------------------------
2. Axillary Nerve injury [16]
Ans.
The axillary nerve arises from the posterior cord of the brachial plexus & has anterior and posterior
branches.
The anterior branch supplies the deltoid
The posterior branch supplies the teres minor and posterior part of the deltoid and terminates
as the cutaneous nerve which supplies the skin over the lower-half of the deltoid
Tests: The patient is asked to abduct his shoulder. Inability to abduct the shoulder, and the absence
of the deltoid becoming taut indicates deltoid paralysis
----------------------------------------------------------------------------------------------------------------------------------------
3. Seddon's classification of nerve injuries [13, 10]
a. Neuropraxia [07, 06, 03]
b. Axonotmesis [05]
Ans.
Seddon classifies nerve injuries into 3 types:
: It is a physiological disruption of conduction in the nerve fibre. No structural changes
occur. Recovery occurs spontaneously within a few weeks, and is complete.
: The axons are damaged but the internal architecture of the nerve is preserved.
Wallerian degeneration occurs. Recovery may occur spontaneously but may take many months.
Complete recovery may not occur.
: The structure of a nerve is damaged by actual cutting or scarring of a segment.
Wallerian degeneration occurs. Spontaneous recovery is not possible, and nerve repair is required.
----------------------------------------------------------------------------------------------------------------------------------------
4. Card test [05]
Ans.
This is done for palmar interossei (adductors) of the fingers which
are supplied by Ulnar Nerve.
Procedure: In this test, the examiner inserts a card between two
extended fingers and the patient is asked to hold it as tightly as
possible while the examiner tries to pull the card out. The power of
adductors can thus be judged.
----------------------------------------------------------------------------------------------------------------------------------------
5. Pointing index [05]
Ans.
 On asking the patient to make a fist, it is noticed that the index finger remains straight.
 Cause of Deformity: occurs due to paralysis of both the flexors (digitorum superficialis and lateral
half of the digitorum profundus) of the index finger
 Seen in: median nerve palsy at a level proximal to the elbow.
 The other fingers can be flexed by the functioning medial side of the flexor digitorum profundus,
supplied by the ulnar nerve.
 Injuries around Shoulder Joint

1. Shoulder Rotator cuff diseases & TB osteomyelitis [21]

a. Rotator cuff Injury [11]
Ans.
Rotator cuff is an anatomical term given to
the group of muscles & their tendons that act
to stabilize the shoulder
Muscles of Rotator Cuff – 4 in no. –
Supraspinatus, Infraspinatus, Teres minor &
Subscapularis.
Rotator cuff diseases are: MCC of
Shoulder pain
Inflammations – Tendonitis, Bursitis
Bone Spur {Acromion rubs on the rotator
cuff & Bursa}
Impingement {tendon is squeezed & rubs against the bone}
Rotator cuff tear
Age related Degenerative Changes – Ex: Frozen shoulder
(adhesive capsulitis)
Features of Rotator cuff injuries: {Cause of Shoulder Pain}
Cause of injury to rotator cuff: due to repetitive use of the upper
limb above the horizontal level (e.g., in throwing sports, swimming,
and weight lifting).
Deposition of calcium in the supraspinatus tendon  calcific
supraspinatus tendinitis
Deposition of calcium  irritates the overlying subacromial bursa
subacromial bursitis
Painful arc – This is a test to detect subacromial impingement of the rotator-cuff
Gradually abduct & internally rotate pt’s shoulder  pain occurs during 60°–120° of abduction
(painful arc syndrome).
This is because the rotator-cuff gets impinged between the head of the humerus & acromion
between this arc of abduction.
Drop-arm sign: seen in complete tear of the rotator-cuff. The examiner abducts the arm of the
patient, while stabilising the scapula with the other hand till 90o of abduction is achieved  the
patient will not be able to hold the arm  Dropped arm
Dawnbarn sign: seen in subacromial bursitis; Press deltoid just below the acromion in an adducted
arm  PAIN;
The pain cannot be elicited by the pressure on the same point when the arm is abducted
because the bursa slips/disappears under the acromion process

TB rarely affect long bones; Tuberculosis of the small bones of the feet & hands is more common.
Clinical Presentation: Bone pain {Calcaneum is a common site} & h/s/o Pulmonary TB in the past
  Spina Ventosa – is a name given to tuber­culosis of the phalanges of hand. The affected phalanx
swells up like a balloon  X-ray revels a lytic lesion distending the phalanx & lot of new bone formation
Diagnosis is done with X-ray – it reveals that bone lysis is out of proportion to the new bone
formation, unlike in pyogenic osteomyelitis
In cases where diagnosis is in doubt  curettage of the lesion and histopathological examination.
Treatment is by rest and ATT.
----------------------------------------------------------------------------------------------------------------------------------------
2. Describe anatomy of upper end of humerus bone. Describe fracture neck of humerus – symptoms,
signs, Tt & complications [15]
Ans.
The proximal end of the humerus consists of the head
articulating with glenoid cavity of the scapula (the
gleno-humeral joint or the shoulder joint proper).
Anatomical neck separates the head from the greater
and lesser tuberosities.
The region below the tuberosities where the globular
upper end of the bone joins the tubular shaft of the
bone is called the surgical neck.
Fractures are more common at the surgical than the
anatomical neck.
:
: elderly women.
: Fall on the shoulder.
: Pain in the shoulder following a fall.
- 4 types depending upon the
construction of the fracture {shaft, head, greater tuberosity
and lesser tuberosity} – Ex: a fracture where the head, the
greater tuberosity, the lesser tuberosity and the shaft, all
have separated, it will be called a four-part fracture.
is by AP and axial X-rays.

 In younger persons with widely displaced fragments 

reduce by manipulation under anaesthesia. Often, open
reduction and internal fixation {with K-wires or modern LCP based special plates} may be required.
 In Elderly with mild # displacement – Immobilise the affected shoulder in a triangular sling. As soon
as the pain subsides, shoulder mobilisation is started.
 In badly comminuted fractures in an elderly  replacement arthroplasty.
:
 Injury to the axillary nerve  paralysis of the deltoid muscle & a small area of anaesthesia over the
lateral aspect of the shoulder. Treatment is conservative, and the prognosis is good.
 Shoulder Stiffness
----------------------------------------------------------------------------------------------------------------------------------------

1) Recurrent dislocation of shoulder [18, 04]

a. Recurrent Anterior Dislocation of shoulder [05]
 b. Anterior Dislocation of shoulder [03]
Ans.
Dislocation of the Shoulder – commonest joint in the human body to dislocate.
:
: A fall on an out-stretched hand with the abducted & externally rotated shoulder
: Direct blow on the front of the shoulder, electric shock or convulsion.
:
Dislocation occurs more commonly in adults, and is rare in children.
Anterior dislocation is much more common than posterior dislocation.
The patient enters the casualty with his shoulder abducted and the elbow supported with opposite
hand.
H/o a fall on an out-stretched hand followed by pain and inability to move the shoulder.
On examination:
Inspection: The patient keeps his arm abducted. The normal round contour of the shoulder joint is
lost, and it becomes flattened & fullness below the clavicle due to the displaced head.
Signs of anterior dislocation:
: Inability to touch the opposite shoulder.
: Because of the flattening of the shoulder, a ruler can be placed on the
lateral side of the arm which simultaneously touches the acromion & lateral condyle of the
humerus.
Posterior dislocation usually occurs following a convulsion; Loss of external rotation is seen
: X-ray of the shoulder

For acute dislocation – reduction is under sedation or general anaesthesia,  immobilisation of the
shoulder in a chest-arm bandage for 3 weeks  shoulder exercises.
Techniques of Reduction of Shoulder Dislocation
 Kocher's manoeuvre – steps: with the elbow flexed to a right angle - TEA-I (Traction, Ext.
rotation, Adduction, Int. rotation)
 Hippocrates manoeuvre – the surgeon applies a firm and steady pull on the semi-abducted arm.
He keeps his foot in the axilla against the chest wall. The head of the humerus is levered back into
position using the foot as a fulcrum.

Early complications: Injury to the axillary nerve.

Late complications: The shoulder is the commonest joint to undergo recurrent dislocation.
:
 Anatomically unstable joint e.g., in Marfan's syndrome;
 Inadequate healing after the first dislocation, or
 An epileptic patient.
: Surgical Options to prevent recurrences are:
: Double-breasting of the subscapularis tendon
: The glenoid labrum & capsule are re-attached to the front of the glenoid rim.
: more expensive cosmetic option with faster and better rehabilitation
: the coracoid process & its attached muscles, is osteotomized at its base and
fixed to lower-half of the anterior margin of the glenoid.
----------------------------------------------------------------------------------------------------------------------------------------
2) Periarthritis of the Shoulder [09, 03]
a. Frozen Shoulder [12, 10]
Ans.
‘Frozen’ Shoulder (Periarthritis Shoulder)
: Idiopathic
Here, the shoulder joint becomes painful & stiff because of the loss of resilience of the joint
capsule due to adhesions between its folds.

Pain and stiffness of the shoulder.

In early stages, the pain is worst at night, and the stiffness limited to abduction and internal
rotation of the shoulder. Later, the pain is present at all times and all the movements of the
shoulder are severely limited.

Self-limiting disease – last for 6-9 months, after which the inflammation subsides, leaving a but
painless shoulder. can be prevented by continuous shoulder mobilising exercises
Administer analgesics, hot fomentation and physiotherapy.
Intra-articular injection of hydrocortisone – to speed up the recovery.
----------------------------------------------------------------------------------------------------------------------------------------
3) Synovial sarcoma [01]
Ans.
Synovial Sarcoma is a malignant tumour, histologically a combination of synovial cells & fibroblasts.
MC Site: knee. It may not necessarily originate from the synovial membrane.
More often, it is extra-articular in origin.
Spread: s via the blood vessels, lymphatics, and along the soft tissue planes.
Treatment – Amputation
Prognosis is poor
 Injuries around Elbow Joint

1. Supracondylar fracture of humerus – mode of injury, C/F, inv. Tt & Complications [21, 19, 16]
a. Supra condylar fracture of elbow [19]
b. Supracondylar fracture in Children – C/F, Mx & complications [12]
Ans.
Supracondylar Fracture of the Humerus is one of the most serious fractures in childhood as it is often
associated with complications.
: The fracture is caused by a fall on an out-stretched hand. As the hand strikes the
ground, the elbow is forced into hyperextension resulting
in fracture of the humerus above the condyles.
: extension or flexion type, depending upon the
displacement of the distal fragment
:
: The child is brought to the
hospital with a history of fall, followed by pain,
swelling, deformity and inability to move the affected
elbow.
: the following signs can be observed:
 Unusual posterior prominence because of the backward tilt of the distal fragment.
 The 3 bony points relationship is maintained {Since the fracture is above the condyles}
 Check for brachial artery injury – Radial and ulnar pulses may be absent
 Check for an injury to the median nerve (pointing index) or the radial nerve (wrist drop).
: The following displacements may be seen on an X-ray
 In an AP view – proximal shift, medial or lateral shift, medial tilt and rotation of the distal fragment.
 In a lateral view – proximal shift, posterior shift, posterior tilt and rotation of the distal fragment.

– Injury to
the brachial artery & Injury to nerves
{median nerve > Radial nerve}.
: Volkmann’s
ischaemia – occurs caused due to
occlusion of the brachial artery.
: Malunion,
Myositis ossificans & Volkmann’s
ischaemic contracture (VIC)

----------------------------------------------------------------------------------------------------------------------------------------
2. Mention the injuries around elbow joint. Describe Fracture neck radius bone – symptoms, signs,
treatment & complications [17, 09, 05]
Ans.

Supracondylar fracture of the humerus Fracture of the head of the radius

Fracture of the lateral condyle of the Fracture of neck of the radius
humerus Fracture of the medial epicondyle of the
Intercondylar fracture of the humerus humerus
Pulled elbow Fracture of the capitulum
Fracture of the olecranon Dislocation of the elbow joint

: occurs in children. It is a valgus injury of the elbow.

 For mild displacements – just immobilisation is done in an above-

elbow plaster slab for 2-3 weeks.
 For severe angulation (> 60°) – reduce by closed manipulation.
 Sometimes, open reduction and fixation with K-wire is required.
: cubitus valgus deformity may occur in a malunited
fracture
----------------------------------------------------------------------------------------------------------------------------------------

1. Monteggia’s Fracture [19, 03]

Ans.
This is a fracture of the upper-third of the ulna with dislocation of the
head of the radius.
: Fall on an out-stretched hand or from a direct blow on
the back of upper forearm.
– depending upon the angulation of the ulna fracture – extension and flexion type.
– X ray

Closed reduction can be tried but this is a very unstable fracture – frequently re-displaces even if it
has been reduced once.
In case, the reduction is not possible or if re-displacement occurs, an open reduction and internal
fixation using a plate is performed.
– Malunion  limitation of elbow & forearm movements
----------------------------------------------------------------------------------------------------------------------------------------

1) Tennis elbow [21, 15, 12]

Ans.
Tennis Elbow (Lateral Epicondylitis)
It occurs due to non-specific inflammation at the origin of the extensor muscles of the forearm
tennis players, activities such as squeezing clothes, carrying a suitcase etc.
: pain and tenderness at the lateral epicondyle of the humerus.
 Pain is aggravated by putting the extensor tendons to a stretch; for example, by palmar-flexing the
wrist and fingers with the forearm pronated.
 X-ray does not reveal any abnormality.
NASAIDs for 1 week  If there is no response, a local injection of hydrocortisone at the
point of maximum tenderness generally brings relief.
 Injuries to Forearm & Wrist

1. Mention injuries around wrist joint. Describe Colle’s' fracture – Definition, mode of injury,
displacement, symptoms, signs, Mx & complications [21, 20, 19, 18, 14, 13]
a. Colle’s fracture – causes, Dx and complications [18, 06]
b. Dinner fork deformity [15]
c. Enumerate the fracture of lower third of radius near wrist joint [07]
Ans.
Injuries around wrist joint
– carpal tunnel syndrome + �
Colles' fracture
: This is a fracture at the distal end of the radius, at its cortico-cancellous junction in adults,
with typical displacement. It is the commonest fracture in people > 40 years of age, and is particularly
common in women because of postmenopausal osteoporosis
: fall on an out-stretched hand
: The following are the displacements seen in Colles' fracture:
 Impaction of fragments
 Dorsal displacement • Dorsal tilt
 Lateral displacement • Lateral tilt
 Supination
 Rarely, the whole of distal fragment is broken into pieces.
:
Symptoms: pain, swelling and deformity of the wrist.
Signs: tenderness and irregularity of the lower end of the radius with a typical
‘dinner fork deformity’.
: The dorsal tilt is the most characteristic displacement &
can be identified on X-ray.

For undisplaced fracture – Immobilisation in a below-elbow plaster cast for 6 weeks

- manipulative reduction & then immobilisation in Colles' cast.
Technique of closed manipulation: Under anaesthesia, grasps the injured hand as if he was
‘shaking hands’  firm longitudinal traction to the hand against the counter-traction by an
assistant at the flexed elbow press the distal fragment into palmar flexion, ulnar deviation &
pronation using thumb of other hand apply below elbow plaster cast {Colles' cast}.
Take an X-ray is taken to check the success of the closed reduction.
Take check X-rays every week for the first 3 weeks in order to detect re-displacement.
Remove plaster after 6 weeks and start joint mobilising and muscle strengthening exercises for the
wrist and fingers.
Modern surgical treatment is to fix these fractures with LCP (Locking compression plate).
– Malunion, Stiffness of the fingers, Sudeck's osteodystrophy, Subluxation of the
inferior radio-ulnar joint, Carpal tunnel syndrome, and Rupture of the extensor pollicis longus tendon.
----------------------------------------------------------------------------------------------------------------------------------------
1. Galeazzi Fracture [19]
Ans.
This injury is the counterpart of the Monteggia fracture-dislocation. Here, there is a fracture of the
lower third of the radius with dislocation or subluxation of the distal radio-ulnar joint
fall on an out stretched hand
The radius fracture is angulated medially
and anteriorly. The distal radio-ulnar joint is disrupted,
resulting in dorsal dislocation of the distal end of the ulna.
X ray

 It is difficult to achieve and maintain perfect reduction by conservative methods (except in

children).
 Adults require open reduction and internal fixation of the radius with a plate.
 The dislocated radio-ulnar joint may automatically fall back in place or may require open reduction.
Malunion  deformity and limitation of supination and pronation
----------------------------------------------------------------------------------------------------------------------------------------
2. Fracture of shaft of radius [15]
Ans.
: The cause of fracture
may be either an indirect force such as a
fall on the hand, or a direct force such as
a ‘lathi’ blow to the forearm.

– X ray. Fractures in children

are often undisplaced and may not have
much signs.

: Infection, Volkmann's
ischaemia, Delayed union and non-
union, Malunion & Cross union.
----------------------------------------------------------------------------------------------------------------------------------------

1. Smith fracture [21]

Ans.
Smith's Fracture (Reverse of Colles' Fracture): This uncommon fracture is seen in adults and in
elderly people.
 It differs from Colles' fracture in that the distal fragment displaces ventrally and tilts ventrally.
 Treatment is by closed reduction and plaster cast immobilisation for 6 weeks.
 Complications are similar to those in Colles' fracture
 Hand Injuries

1. Mallet finger [15, 12, 08, 04]

Ans.
Mallet finger (Baseball finger)
Mode of injury: results from the sudden passive flexion of the distal IP joint so that the extensor
tendon is avulsed from its insertion at the base of the distal phalanx. Sometimes it takes a fragment of
bone with it.
Clinically, distal phalanx is in slight flexion.
Treatment is by immobilising the DIP joint in hyperextension with the help of an aluminium splint or
plaster cast
----------------------------------------------------------------------------------------------------------------------------------------
2. Fracture scaphoid [01]
Ans.
A scaphoid fracture is more common in young adults. It is rare in children and in elderly people.
It may be either a crack fracture or a displaced fracture.
fall on an outstretched hand
:
Pain and swelling over the radial aspect of the wrist
On examination – tenderness in the scaphoid fossa (anatomical snuff box).
: X-ray oblique view of the wrist besides AP & Lateral view

Immobilise in a scaphoid cast for 3-4 months.

In widely displaced fractures – open reduction and internal fixation using a special compression
screw (Herbert's screw) is required.
Avascular necrosis; Delayed and non-union & Wrist osteoarthritis
----------------------------------------------------------------------------------------------------------------------------------------

1) Trigger finger [21, 20, 19, 18]

Ans.
: is a condition resulting from the constriction of the fibrous digital sheath, so
that free gliding of the contained flexor tendon does not occur.

 Pain & swelling at the base of the affected finger

 The swollen segment of the tendon does not enter the sheath when an attempt is made to
straighten the finger from the flexed position. This is called ‘locking of finger’.
 This locking can be overcome either by a strong effort in which case the finger extends with a snap-
like trigger of a pistol or by extending the finger passively with other hand.

 In early stages, local ultrasonic therapy provides relief.

 In a long-standing problem, a local injection of hydrocortisone relieves the pain.
 Pelvic Fractures

1) Fracture pelvis – classify, etiology, symptoms, signs, complications & Mx [03, 01]
Ans.
– Road traffic accidents {MCC}, falls from great heights,
crushing accidents etc.

:
The pelvic compression test is a useful screening test in all
cases of RTA.
Shortening of one of the lower limbs - in displaced pelvic fractures.
There may be a haematoma in the region of pubic symphysis or at the back, in the region of Sacro-
iliac joints.
Palpation may reveal a localised tenderness or crepitus.
There may be signs due to
associated injury to the
urethra, bladder or
intestine etc.,
There may be anaesthesia
or weakness of one leg
due to injury to the sciatic
plexus.

– Rupture of
urethra & bladder; Injury to
rectum or vagina; Injury to
major vessels & Nerves;
Rupture of the diaphragm

:
 Injuries around Hip

1. Fracture neck of femur – classify, etiology, C/F, Dx, Mx & Complications [19, 12, 08, 07, 06]
a. Avascular necrosis of hip – C/F & Mx [21]
b. Avascular necrosis of head of femur – pathogenesis, C/F & Mx [20, 16]
c. Classify fractures around the proximal femur. Describe Intracapsular fracture neck of femur –
C/F, Mx in a 65-year-old female & Complications [15]
Ans.
:
Anatomical classification – 3 types – based on location: Subcapital {just below the
head}; Transcervical {middle of the neck}; Basal {at base of the neck}. �
Pauwel’s classification – 3 types {type I-III} – based on the
angle of inclination of the fracture in relation to the
horizontal plane (Pauwel’s angle) �
Garden’s classification: This is based on the degree of
displacement of the fracture (mainly rotational
displacement) – 4 stages� �

 In elderly people, the fracture occurs with a seemingly

trivial fall like slipping on the floor, missing a step etc.
due to a/w Osteoporosis esp. in females
 In young people – RTA
:
Pain in the groin and inability to move the limb or bear weight on the limb following a ‘trivial’ injury
Examination reveals the following:
External rotation of the leg, the patella facing outwards.
Slight Shortening of the leg.
Tenderness in the Scarpa’s triangle.
Attempted hip movements painful, and associated with severe spasm.
Active straight leg raising not possible.
X-ray of pelvis with
both hips. The following can be seen on
affected hip:
Break in the medial cortex of the neck.
External rotation of the femur is evident;
the lesser trochanter appear more
prominent
Overriding of greater trochanter, so that it
lies at the level of the head of the femur.
Break in the trabecular stream.
Break in Shenton’s line.
�
 Non-union
Avascular necrosis: Occurs due to loss of blood supply.
This may, in addition, be a cause of non-union.
Leads to deformity  osteoarthritis
MRI is the best investigation for this purpose.
Treatment:
In young patients treatment options are: arthrodesing the hip, bipolar arthroplasty, Meyer’s
procedure or rarely, total hip replacement (THR).
In elderly patients, a hemi-replacement arthroplasty is performed.
If there is an associated damage to the hip, a total hip replacement may be preferred.
Osteoarthritis: It develops a few years following fracture of the neck of femur.
----------------------------------------------------------------------------------------------------------------------------------------
2. Trochanteric Fracture of Hip – mechanism of injury, C/F & Mx [06]
Ans.
Fractures in the inter trochanteric region of the proximal femur, involving either the greater or the
lesser trochanter or both.
:
– sideway fall or a blow over the greater trochanter.
– violent trauma, as in a road traffic accident.
:
Pain in the region of the groin and an inability to move the leg.
There will be swelling in the region of the hip, and the leg will be
short and externally rotated.
Tenderness over the greater trochanter.
: Diagnosis is easy on an X-ray.
: to maintain a normal femoral neck-shaft angle during the process of union.
Contrary to fracture of the neck of the femur, trochanteric fractures unite readily.
Conservative methods: Russell’s traction and skeletal traction in a Thomas splint
Internal fixation – preferred in elderly; The fracture is reduced under X-ray control and fixed with
internal fixation devices like:
(i) Dynamic Hip Screw (DHS) (ii) Ender’s nails & (iii) Nails – gamma nail, Proximal femoral nail (PFN).
External fixation – done in patients with bed sores & for those who are unfit for a major operation
Malunion
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1) Perthes’ disease [18, 16, 13]

Ans.
Perthes’ disease – aka Coxa plana & Pseudocoxalgia – is an osteochondritis of the
epiphysis of the Femoral head
Cause: it is not definitely known.
High Risk: Boys in the age group of 5-10 years
Due to recurrent ischemia of femoral head precipitated by episodes of synovitis  the femoral
head becomes partly or wholly avascular and deformed
 4 groups have been described by Catterall based on the extent of involvement of the head.
Pathologically, the disease progresses in 3 ill-defined stages:
1) Stage of synovitis;
2) Stage of trabecular necrosis; and
3) Stage of healing.
C/F: The child presents with pain in the hip, radiating to the knee & a/w limping or hip stiffness
Investigations:
 X ray – reveals collapse & sclerosis of the epiphysis of femoral head +  Hip joint space
 Bone scan – reveals  uptake by the head of the femur
Treatment:
Aim: Prevent the bone from mis-shapening
Head containment: The head is kept inside acetabulum while the revascularisation occurs.
Conservative methods – plaster, splint etc.
Surgery - Containment osteotomy
----------------------------------------------------------------------------------------------------------------------------------------
2) Trendelenburg test [08, 05]
Ans.
: The ASISs of both sides should be exposed.
When patient stand on the normal leg, the opposite ASIS will be
lifted up i.e., the pelvis will be tilted towards the side bearing
weight.
Now, the patient is asked to stand on the affected side  the
opposite ASIS will dip down. In order to avoid falling, the patient
will tilt his torso to the affected side and thus balance himself.
:
The tilting of pelvis is possible due to ‘effective contraction’ of the
abductor muscles of the hip (mainly gluteus medius).
Any failure in the effectivity of the abductor mechanism causes dipping of the ASIS on the opposite
(normal) side.
This could occur if:
(a) there is no fulcrum – e.g., dislocation of the hip, destruction of the head;
(b) ineffective lever-arm (the neck of the femur) – e.g., fracture of the neck of the femur;
(c) ineffective contraction of abductor muscles – e.g., weakness of the muscles due to polio
 Fracture Shaft of Femur

1. Fracture shaft femur – classify, C/F, radiological features & Mx [21]

a. Compound, Comminuted fracture shaft of Femur – signs, symptoms & Mx [03]
Ans.
A fracture of the shaft of the femur is usually sustained by a severe violence, as may occur in a road
accident. The force causing the fracture may be indirect (twisting or bending force) or direct (traffic
accidents)
Classification:
 It can involve upper, middle or lower shaft;
 It can be transverse, oblique etc.
Clinical features: The patient presents with a history of severe violence followed by classic signs
of fracture in the region of the thigh (pain, swelling, deformity, abnormal mobility etc
Radiological examination: X-rays for whole femur & pelvis should be done.
Treatment
Conservative methods – preferred in open fractures &
in children:
– Skin traction is sufficient in children, but
skeletal traction is required in adults
 Skeletal traction is given by a Stienmann pin
passed through the upper-end of tibia.
 Gallow's traction used in children <2years
: This is a plaster cast incorporating part of
the trunk and the limb.
Operative methods: The fracture may be reduced by closed {under x-ray control} or open methods
 Closed Interlock nailing is the preferred method.
 Plating (fixing with a thick strip of metal) is preferred in cases where good hold is not possible
by a nail. Minimum of 16 cortex hold (8 screws) is desirable.
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1) Sciatica [12]
a. Sciatic nerve injury [17]
Ans.
Sciatica is a symptom and not a diagnosis.
It means a pain radiating down the back of the thigh and calf.
Broadly, sciatica can either be because of inflammation of the
sciatic nerve or because of compression of one of the roots
constituting the sciatic nerve
Degenerative arthritis and disc prolapse are the common causes.
 Injuries around Knee joint
1. Anterior cruciate ligament tear of Knee – C/F & Mx [05]
a. Cruciate ligaments of knee [21]
Ans.
There are two cruciate ligaments in the knee
 Anterior cruciate – Prevents anterior gliding of the tibia on the femur
 Posterior cruciate – Prevents posterior gliding of the tibia on the femur
: ACL tear occurs due to twisting force on a semi-flexed knee
 Often the injury to medial collateral ligament, medial meniscus and anterior cruciate ligament
occur together. This is called O'Donoghue triad.
 PCL is damaged if the anterior aspect of the tibia is struck with the knee semi-flexed so as to force
the tibia backwards on to the femur.
:
Pain and swelling of the knee
H/o trauma, followed by a sound of something tearing.
Anterior drawer test & Lachmann test – to detect ACL injury
Posterior drawer test – to detect PCL injury.
:
A plain X-ray may be normal, or a chip of bone avulsed from the
ligament attachment may be visible.
Stress X-rays – can demonstrate an abnormal opening-up of the
joint
MRI is a non-invasive method of diagnosing ligament injuries.
Other investigation: Arthroscopic examination may be needed in cases where doubt persists.

: Aspirate the haematoma & immobilise the knee in a cylinder cast. After a
few weeks, the swelling subsides, and adequate strength can be regained by physiotherapy.
: These are indicated in multiple ligament injured knee, especially in young
atheletes. The operation is usually performed 2-3 weeks after injury after the acute phase
subsides. It consists of the following:
a) Repair of the ligament – done for fresh, grade III collateral ligament injuries.
b) Reconstruction – The treatment of choice is arthroscopic ACL reconstruction
 Done in cases of ligament injuries presenting late with features of knee instability.
 A ligament is ‘constructed’ using patient's tendon or fascia lata or a synthetic ligament.
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1. Genu Valgum & it’s causes [19, 18]

Ans.
This is a condition where the
knees are abnormally approximated and the ankles abnormally
divergent
Causes: idiopathic {MC}
Clinical features:
 Physiological genu valgum appears at the age of 2-3 years and
nearly always corrects by age of 6.
 It may be associated with flat feet.
 The degree of deformity is estimated by measuring the inter-
malleolar distance
 In genu valgum secondary to a disease such as rickets, there will
be findings suggestive of the primary disease.
Treatment:
 Spontaneous recovery occurs in most idiopathic cases.
 A medial shoe raise can be prescribed – to satisfy the anxious
parents.
 If the inter-malleolar distance > 10 cm by the age 4, the child may need an operation 
supracondylar closed wedge osteotomy is performed.
----------------------------------------------------------------------------------------------------------------------------------------
2. Fracture Patella [19, 12]
Ans.
: once fracture occurs by a direct violence, a simultaneous contraction of the
quadriceps pulls the fragments apart, and results in a separated fracture of the patella.

Pain and swelling {haemarthrosis} over the knee.

A crepitus is felt in a comminuted fracture.
In displaced fractures, one may feel a gap between the fracture fragments.
The patient will not be able to lift his leg with the knee in full extension
There may be bruises over the front of the knee – a tell tale sign of direct trauma.
: AP and lateral X-rays of the knee are sufficient in most cases. In some
undisplaced fractures, a ‘skyline view’ of the patella may be required.

a) Undisplaced fracture – Analgesics + cylinder cast from the groin to just above the malleoli, with the
knee in full extension should be given for 3 weeks, followed by physiotherapy.
b) Clean break with separation of fragments (two-part fracture): The operation consists of reduction
of the fragments, fixing them with tension-band wiring (TBW) and repair of extensor retinaculae.
Consider Patellectomy if reduction is not possible. Such operations on the patella are followed by
support in a cylinder cast for 4-6 weeks.
c) Comminuted fracture – excision of the patella (patellectomy) is the preferred option. But,
reconstructions can also be considered (patella saving operations).

 Knee stiffness- due to intra & peri-articular adhesions – Treat by physiotherapy.

 Extensor weakness – due to inadequate repair of the extensor apparatus or due to quadriceps
weakness.
 Osteoarthritis: Patello-femoral osteoarthritis occurs a few years after the injury.
----------------------------------------------------------------------------------------------------------------------------------------
3. Dislocation of knee [19, 04]
Ans.
: This rare injury results from severe violence to the knee so that all of its supporting ligaments
are torn. It is often a/w injury to the popliteal artery.
 is by reduction followed by immobilisation in a cylinder cast.
 Multiple ligament reconstruction can be considered.
----------------------------------------------------------------------------------------------------------------------------------------
4. Cubitus varus deformity [11]
Ans.
: Malunion of a supracondylar fracture
: Gun stock deformity.
: it is a cosmetic problem, usually without much functional impairment.
Mild deformity may not require treatment
Severe deformity is treated with a supracondylar corrective osteotomy (French osteotomy).
----------------------------------------------------------------------------------------------------------------------------------------
5. Loose Bodies in knee [03]
Ans.
: Fractured osteophyte (osteoarthritis) knee osteochondritis, osteochondral fractures,
synovial chondromatosis etc.
: sudden locking of the joint. Patient can feel the loose body within the joint.
: Most loose bodies are radiopaque and can be seen on plain X-rays. In some, an
arthroscopic examination may be required.
is removal of the body arthroscopically or by opening the joint.
----------------------------------------------------------------------------------------------------------------------------------------
6. Bursae around the knee [02]
a. Bursa [21, 08]
b. Morant-Baker Cyst [16, 04]
c. Baker’s cyst [21, 12]
Ans.
Bursa is synovial fluid-filled sac that helps to reduce the friction between a bone & a muscle or a
bone & a tendon
Different bursae in relation to the knee, which may present as swelling are:
causes painless oval swelling at the postero-medial aspect of the knee;
(Clergyman’s knee) lying deep to the ligamentum patellae;
(Housemaid’s knee) lying in front of the patella;
Morrant-Baker's cyst – a posterior herniation of the synovial membrane in the popliteal fossa. A
swelling can be seen distending the suprapatellar pouch, giving rise to a horseshoe shaped
swelling, and is suggestive of effusion into the knee
----------------------------------------------------------------------------------------------------------------------------------------

1. Determination of muscle power of knee joint [17]

Ans.

----------------------------------------------------------------------------------------------------------------------------------------
2. Recurrent Dislocation of Patella [11]
Ans.
Generally occur during adolescence

 excessive joint laxity; ruptured medial patello-femoral ligament

 a small patella;
 a patella alta (i.e., the patella is high–lying in the shallower part of intercondylar groove);
 genu valgum.
– operative reconstruction aimed at correcting the underlying cause
 Hauser's operation – Insertion of the patellar tendon on the tibial tuberosity is shifted medially and
downwards so that the line of pull of the quadriceps shifts medially.
 Prof. Baksi operation – pes anserinus is transferred to lower pole of the patella to provide a
‘checkrein’ effect.
 The current trend is arthroscopic assisted operations
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3. Describe internal derangement of knee joint. [08]
Ans.
 Internal derangement of the knee (IDK) is a term used to group all the other, non-bony injuries of
the knee.
 These consist of ligament injuries, meniscus injury and patello-femoral problems.
 Injuries to Leg, Ankle & Foot

1. Discuss the injuries around the ankle joint and their treatment [14]
a. Pott’s Fracture [04]
b. Discuss the mechanism of injuries to the Ankle Joint, complications & Mx [03]
Ans.
Pott’s Fracture refers to fractures of the bones forming the ankle joint
The Lauge-Hansen classification is based on the mechanism of injury to ankle joint:

h/o a twisting injury to the ankle followed by pain and swelling.

Swelling and tenderness may be localised to the area of injury (bone or ligament).
Crepitus may be noticed if there is a fracture.
The ankle may be lying deformed (adducted or abducted, with or without rotation).
: AP and lateral X-rays are taken

Stiffness of the ankle after immobilisation in plaster – Treatment is ankle exercises.

Osteoarthritis – Since most ankle fractures involve the articular surfaceslead to wear and tear of
the articular cartilage  degenerative osteoarthritis. Management is eliminating the joint by fusing
the talus to the tibia (ankle arthrodesis) in severe cases.
is to achieve anatomical reconstruction
– protect the ankle with a below-knee plaster or braces
: Aim of treatment is to ensure anatomical reduction which can be
achieved by:
– reduction by manipulation under general anaesthesia. Once reduced, a
below-knee plaster cast is applied. Check X-rays are taken frequently  the plaster is removed
after 8-10 weeks  physiotherapy to regain movement at the ankle
– to achieve perfect alignment which allows early motion of the ankle joint
Internal fixation – techniques used for internal fixation depend upon the type of fracture. Ex:
 For Transverse Malleolus Fracture – tension-band wiring
 For Oblique fracture – compression screws
 External fixation – done in cases where closed methods cannot be used e.g., open fractures with
bad crushing of the muscles and tendons, with skin loss around the ankle.
----------------------------------------------------------------------------------------------------------------------------------------

1) Ruptured Tendo Achilles [03]

Ans.
Achilles’ tendon is the largest tendon in the body
Origin from gastrocnemius and soleus muscles & insert on calcaneal tuberosity
: social violence, accidental cut injury {bathroom injury, RTA etc.
: tenderness, crepitations, warmth, swelling, nodularity, palpable defects &
+ve Thompson test
: x-ray of the calcaneus shows an
avulsion fracture at the insertion of the Achilles
tendon; Ultrasound can also be done
:�
- Debride and approximate
tendon ends; Beware of sural nerve

----------------------------------------------------------------------------------------------------------------------------------------

1. Flat Foot [15]

Ans.
Flat Foot is a foot with less developed longitudinal arches
Either of the parents usually have flat feet. Such individuals lead a
normal life except that they are prone to developing foot strain
Diagnosis: can be done by taking an X-ray of the foot (lateral view)
Treatment:
In infantile flat foot – arches develop as the child grows, and no
special treatment is required
In mild cases, the footwear is modified to provide an arch support at mid foot.
In severe cases, corrective surgery is required.
----------------------------------------------------------------------------------------------------------------------------------------
2. Jones Fracture [11]
Ans.
This is a fracture at the base of the 5th metatarsal, caused by the pull exerted by the tendon of the
peroneus brevis muscle inserted on it.
Clinically, there is pain, swelling and tenderness at the outer border of the foot
Diagnosis is easily confirmed on X-ray
Treatment is by a below-knee walking plaster cast for 3 weeks.
 Infections of Bone & Joint

1) Acute osteomyelitis – etiopath, C/F, Complications, inv. DDx & Tt [18, 09, 05, 02]
a. Treatment of acute suppurative arthritis [07]
Ans.
It is defined as inflammation of the bone & marrow secondary to infection with bacteria (MC), virus,
fungi or parasites

Causative organisms: Staphylococcus aureus (MC), Streptococcus and Pneumococcus

Site: Lower femoral metaphysis (MC), upper tibial, upper femoral and upper humeral metaphyses.
These organisms reach the bone via the blood circulation
↓
get lodged in the metaphysis.
↓
inflammatory reaction of bone in response to the bacteria.
↓
bone destruction and production of pus
↓
pus spreads in the following directions
a) Along the medullary cavity: Pus trickles along medullary cavity thrombosis ischemia.
b) Out of the cortex: Pus travels along Volkmann’s canalssub- periosteumdamage to the
periosteal blood supply to that part of the bone avascular segment of bone (sequestrum).
↓
Pus under the periosteum generates sub-periosteal new bone (periosteal reaction).
↓
Eventually the periosteum is perforated abscess
↓
Unattended abscess discharging sinus
↓
pus can spread to the joint, and cause acute pyogenic arthritis

 Acute onset of pain and swelling at the end of a bone

 Fever, dehydration
 One may find a primary focus of infection elsewhere in the body (tonsils, skin, etc.).
 In later stages, one may find an abscess in the muscle or subcutaneous plane.
 There may be swelling of the adjacent joint, because of either sympathetic effusion or concomitant
arthritis DIFFERENTIAL DIAGNOSIS:
: • Acute septic arthritis
• Acute rheumatic arthritis
 Blood: PMNL↑ and ESR↑.
• Scurvy
 Blood culture – reveal the causative organism. • Acute poliomyelitis
 X-rays: The earliest sign to appear on the X-ray is a periosteal new bone deposition
:This can be divided into two types
1. General complications – septicaemia and pyaemia.
2. Local complications – because of delay in diagnosis, and inadequate treatment – Chronic
osteomyelitis; Acute pyogenic arthritis; Pathological fracture & Growth plate disturbances
 If the child is brought within 48 hours of the
onset of symptoms:
• Rest the limb in a splint or by traction
• Antibiotics: In children <4 months of age,
a combination of Ceftriaxone and
Vancomycin is given.
In older children, a combination of
Ceftriaxone and Cloxacillin is given
• General building-up of the patient
 Rehydrated with intravenous fluids.
 Weight bearing is restricted for 6-8 weeks
If the child is brought after 48 hours of the
onset of symptoms:
• Ultrasound to detect deep collection of
pus.
• Surgical exploration and drainage is the
mainstay of treatment at this stage.
A drill hole is made in the bone in the region
of the metaphysis drainage is obtained. A
swab is taken for culture and sensitivity. The
wound is closed over a sterile suction drain.
Antibiotics are continued for 6 weeks.

----------------------------------------------------------------------------------------------------------------------------------------
2) Chronic pyogenic osteomyelitis – C/F, complications & Mx [11]
a. Chronic osteomyelitis [14, 10]
Ans.
ETIOLOGY:
a) Delayed and inadequate treatment of acute osteomyelitis
b) Highly virulence of organism
c) Reduced host resistance
CLINICAL FEATURES:
A chronic discharging sinus (MC)
The onset of sinus may be traced back to an episode of acute osteomyelitis during childhood.
Often sinuses heal for short periods, only to reappear with each acute exacerbation.
Pain is aggravated during acute exacerbations.
Generalised symptoms of infection such as fever etc., are present only during acute exacerbations.
COMPLICATIONS
1. An acute exacerbation or ‘flare up’ of the infection occurs commonly.
2. Growth abnormalities:
Shortening, when the growth plate is damaged.
Lengthening because of increased vascularity of growth plate due to nearby osteomyelitis.
3. Pathological fracture may occur through a weakened area of the bone.
4. Joint stiffness may occur because of scarring of soft tissues around the joint.
5. Sinus tract malignancy is a rare complication.
6. Amyloidosis: As with all other long-standing suppurations (late complication)
TREATMENT of chronic osteomyelitis is primarily surgical. Abx are useful only during acute
exacerbations and during post-op period.
:
Sequestrectomy: This means removal of the sequestrum.
Saucerisation – the cavity is converted into a ‘saucer’ by removing its wall.
This allows free drainage of the infected material.
Curettage until the underlying normal-looking bone is seen.
Excision of an infected bone: In a case where the affected bone can be
excised en bloc without compromising the functions of the limb.
Amputation: if the sinus undergoes a malignant change.
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1. Brodie's abscess – sites & C/F [17, 16, 15, 14]
Ans.
It is a special type of osteomyelitis in which the body’s defense mechanisms
have been able to contain the infection so as to create a chronic bone abscess
containing pus or jelly-like granulation tissue surrounded by a zone of
sclerosis.
:
Seen in young patient – A deep boring pain which become worse at night,
on walking and is relieved by rest
Sites: metaphysis of Upper end of the tibia and lower-end of the femur.
Examination may reveal tenderness and thickening of the bone.
– circular or oval lucent area surrounded by a zone of sclerosis. The rest of the
bone is normal.
– Surgical evacuation and curettage is performed under antibiotic cover.
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2. Septic arthritis of knee & its’s etiopath [15, 06, 02]
Ans.
Infection of the knee Joint
It is more common in children, and males are more susceptible.
• Predisposing factors: poor hygiene, poor resistance, diabetes etc.
• Causative organism: Staphylococcus aureus (MC), Streptococcus Pneumococcus and Gonococcus.
• Organism reaches the joint inflammatory response in the synovium exudation of fluid within
the joint Joint cartilage is destroyed.
• Outcome varies from complete healing to total destruction of the joint (ankylosis).

 In Acute form: severe throbbing pain, swelling and redness of the affected joint, high-grade fever
and malaise, the child is unable to use the affected limb.
 In Subacute form: painful limp & low-grade fever.

reveal joint space & a soft tissue shadow

is useful in detecting collection in deep joints such as the hip and shoulder
shows leucocytosis, ESR↑. A blood culture may grow the causative organism.
is the quickest and the best method
: TB arthritis, Haemophilia, RA, other causes of acute arthritis

In its early stage – confirm with joint aspiration  start on IV Ceftriaxone and Cloxacillin  put
joint to rest with a splint or traction.
In late stages – arthrotomy & extensive debridement of the joint  immobilise in the position of
optimum function, so that as the disease heals, ankylosis occurs in that position
: Deformity and stiffness, Pathological dislocation, Osteoarthritis
----------------------------------------------------------------------------------------------------------------------------------------
3. Sequestrum [07]
a. Ring Sequestrum [13]
Ans.
Sequestrum is a piece of dead bone, surrounded by Type of Sequestrum Disease
infected granulation tissue trying to ‘eat’ the Tubular Pyogenic
sequestrum away. Ring External fixator
Black Actinomycosis
It appears pale and has a smooth inner and rough
Coralliform Perthe’s disease
outer surface because the latter is being constantly
Coke Tuberculosis
eroded by the surrounding granulation tissue.
Sandy Tuberculosis
Feathery Syphillis

----------------------------------------------------------------------------------------------------------------------------------------

1. Synovitis [06]
Ans.
Synovitis refers to inflammation of the synovial membrane of synovial joints
: arthritis, gout rheumatoid arthritis, lupus, etc.
: joint tenderness or pain, swelling and hard lumps
: determine whether it’s true synovitis or if it is actually caused by an inflammation of the
tendons, referred to as tendonitis
: NSAIDs  steroid injection
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2. Involucrum [05]
Ans.
 Involucrum is the dense sclerotic bone overlying a sequestrum.
 There may be some holes in the involucrum for pus to drain out. These holes are called cloacae.
 The bony cavities are lined by infected granulation tissue
 TB of Bone & Joints

1. Caries Spine – etiopath, C/F, radiological features & Complications. How would you treat 10-year-
old boy with TB of D10 – D11? [19]
a. Pott’s spine [16]
b. TB of Dorsal spine at D9 level – Mx & Complications [11]
c. Tuberculous spondylitis (Pott's disease) – C/F & Mx [09]
d. TB of spine at various levels – pathology, C/F & Mx [05, 04]
e. Classify Gibbus. Describe C/F & Mx of TB T12-L1 spine [03, 02]
Ans.
The spine is the commonest site of bone and joint tuberculosis; the Dorso-lumbar region being the one
affected most frequently.
TB of the spine is always secondary.
The bacteria reach the spine via the haematogenous route, from the lungs or lymph nodes.
It spreads via the para-vertebral plexus of veins i.e., Batson's plexus.
Granulomatous inflammation  erosion of the margins of these vertebrae.
This results in disc degeneration, and as the process continues, complete destruction.
Weakening of the trabeculae of the vertebral body results in collapse of the vertebra
Types of vertebral tuberculosis: Lesions in the vertebrae may be of the following types:

a) Paradiscal (MC) b) Central c) Anterior d) Posterior

Back Pain: It may be a ‘radicular’ pain i.e., a pain radiating along a nerve root.
Para-vertebral muscle stiffness
Cold abscess  compression  dysphagia in TB of the cervical spine
Paraplegia.
Deformity especially in children, by a gradually increasing prominence of the spine – a gibbus.

• Gait – patient takes short steps in order to avoid jerking the spine
• Attitude and deformity: stiff & straight neck. In dorsal spine TB, part of the spine becomes
prominent (gibbus or kyphus). military
• Para-vertebral swelling – cold abscess
• Tenderness – on the side of the spinous process in an attempt to rotate the vertebra
• Limited spinal movement
• Neurological examination

1. X-ray examination –
  Chest X-ray for primary focus or an X-ray of the abdomen –
 KUB, if a psoas abscess is suspected. Following features can be seen:
Reduction of disc space: This is the earliest sign in the paradiscal type of TB
Destruction of the vertebral body  angular kyphotic deformity.
Evidence of cold abscess: Paravertebral abscess, Retropharyngeal abscess etc
Signs of healing: Areas surrounding the lytic lesion show sclerosis, the density of the affected
bones improves.
2. CT scan – This is a very useful investigation in cases presenting as ‘spinal tumour syndrome’
3. MRI is the investigation of choice to evaluate the type and extent of compression of the cord

Cold abscess: This is the commonest complication of TB of the spine.

Neurological compression: 1st clinical symptom being a neurological deficit.

: provide rest to the spine during the acute phase, followed by guarded mobilisation
: Minerva jacket or a collar may be given for immobilising the cervical spine.
: As the patient improves, he is allowed to sit and walk while the spine is supported in
a collar for the cervical spine, or an ASH brace for the dorso-lumbar spine. The patient is weaned
off the brace once bony fusion occurs. He is advised to avoid sports for 2 years
----------------------------------------------------------------------------------------------------------------------------------------

1. Tuberculosis of knee [15, 12, 10]

Ans.
Etiopathogenesis: The disease begins in the synovial membrane (synovial tuberculosis)hypertrophy
of the synovium spreads under and over the cartilage and destroys itcartilage detach, leaving the
bone exposed.
 Long standing distension of the joint & destruction of ligaments subluxation of the tibia
If untreated, healing is by fibrosis (fibrous ankylosis).
Clinical Features: Age group of 10-25 years
 Knee joint is swollen with Cold abscess.
 Atrophy of the thigh muscles.
 Sinus: There may be discharging or healed sinuses.
 Deformity: In early stages, there is a mild flexion deformity of the knee because of effusion in the
knee, and muscle spasm. Later, triple displacement (flexion, posterior subluxation & external
rotation) occurs due to ligament laxity.
 Movements: The movements at the joint are limited.
Investigations
 X-ray reveals soft tissue shadow corresponding to the distended knee.
 In advanced stages, triple subluxation with cavitatory bone lesions may be present.
Treatment
Conservative treatment:
 Antitubercular chemotherapy
 Rest the knee by applying below-knee skin traction or an above-knee POP slab.
Operative treatment: Synovectomy; Joint debridement; Arthrodesis {in advanced cases}
----------------------------------------------------------------------------------------------------------------------------------------
2. Tubercular Dactylitis [07]
Ans.

----------------------------------------------------------------------------------------------------------------------------------------

1) Cold abscess [15]

Ans.
Cold abscess refers to a collection of pus and tubercular debris from a diseased vertebra.
It is called a cold abscess because it is not associated
with the usual signs of inflammation – heat, redness
etc., found with a pyogenic abscess.
The tubercular pus can track in any direction from the
affected vertebra.
:
 A small cold abscess may subside with anti-
tubercular treatment.
 Abscesses presenting superficially may need
Aspiration or Evacuation
 A psoas abscess can be drained extra-peritoneally
using a kidney incision
 Congenital Talipes Equino Varus

1. Congenital Talipes Equinovarus (CTEV) [21, 20, 14, 10, 09, 03]
a. Club foot [09]
Ans.
CTEV is a congenital deformity where one or both feet have the shape of a club with the sole of the
foot facing inwards & backwards.
Aetiology of Idiopathic clubfoot Aetiology of Secondary clubfoot
a) Mechanical theory: The ↑intrauterine
a) Paralytic disorders: In a case where there is a
pressure forces the foot against the wall of
muscle imbalance (invertors and plantar flexors are stronger
the uterus in the position of the deformity.
than the evertors and dorsiflexors. Ex: In polio, spina
b) Ischaemic theory: Ischaemia of the calf
bifida, myelodysplasia and Freidreich’s ataxia.
muscles during intrauterine life deformities.
b) Arthrogryposis multiplex congenita (AMC):
c) Genetic theory: Some genetically related
This is a disorder of defective development of
disturbances in the development of the foot
the muscles which are fibroticdeformities
deformity
Clinical Features: C A V E = Cavus of 1st toe; Adduction; Varus & Equinus
 Size of the foot is smaller.
 Foot is in Equinus, varus and adduction. Empty heel sign
 Heel is small in size; the calcaneum may be felt with great difficulty.
 Deep skin creases on the back of the heel and on the medial side of the sole.
 Bony prominences felt on the lateral side of the foot, the head of the talus and lateral malleolus.
 Outer side of the foot is gently convex. There are dimples on the outer aspect of the ankle. Talar head sign
Treatment – to correct the deformity & maintain the correction.
Methods of Correcting Deformity
Non-operative methods
ponsetti method - C AV E Operative methods
{for mild deformity}
 Manipulation alone – for a
 Postero-medial soft tissue release (PMSTR)
newborn, the mother is
 Tendon transfers
taught to manipulate the foot
 Dwyer's osteotomy (of the calcaneum)
after every feed. The foot is
 Dilwyn Evan's procedure: PMSTR + calcaneo-cuboid fusion. It
dorsiflexed and everted over a
is used for a neglected clubfoot in children between 4-8 yrs.
period of roughly 5 minutes.
 Wedge tarsectomy – for children between 8-11 years
For minor deformities
 Triple arthrodesis for >12 years.
 Manipulation and POP for
 Ilizarov's technique
older children
Methods of maintenance of the correction
• CTEV splints
• Denis-Brown splint
• CTEV shoes

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2. Congenital deformities of foot [21, 19, 17]
Ans.
Clubfoot (talipes equinovarus), “rocker deformity” (over-corrected clubfoot), flatfoot, metatarsus
varus, and pes cavus.
 Congenital Dislocation of Hip

1. Posterior Dislocation of Hip Joint – mechanism of injury, C/F & Mx [09]

Ans.
The head of the femur is pushed out of the acetabulum posteriorly
: violence directed along the shaft of the femur, with the hip flexed –
Ex: in car accidents, occupant of the car is thrown forwards and his knee strikes against the
dashboardThe force is transmitted up the femoral shaft  posterior dislocation of the hip. It is,
therefore, also known as dashboard injury.
:
h/o severe trauma followed by pain, swelling & deformity (flexion, adduction & internal rotation).
O/E: head of the femur felt in the gluteal region
reveals that the femoral head is out of the acetabulum. The thigh is internally rotated so that
the lesser trochanter is not seen. Shenton’s line is broken.
:
 Reduction of a dislocated hip is an emergency, since longer the head remains out, more the
chances of it becoming avascular.
 Reduce the hip by manipulation under general anaesthesia.
 Open reduction is required in cases where closed reduction fails
: Injury to the sciatic nerve, Avascular necrosis of the femoral head, Osteoarthritis &
Myositis ossificans
----------------------------------------------------------------------------------------------------------------------------------------

1. Congenital dislocation of the Hip [06, 04, 02]

a. Screening for DDH (Developmental Dysplasia of Hip) in Children [15]
Ans.
Congenital dislocation of the Hip {aka DDH} refers to a spontaneous dislocation of the hip occurring
before, during or shortly after birth

Hereditary predisposition to joint laxity

Hormone induced joint laxity by relaxin
Breech malposition
– CDH is more common in 1st born babies, more on the left, more
common in females (M: F=1:5); the following tests can be done to confirm clinically:
 Barlow's test – done to confirm dislocatable Hip - 2 step test:
 1st step is Adduction: Dislocatable hip is dislocated (first click)
 2nd Abduction: Dislocated hip is reduced (second click)
 Ortolani's test – done in Dislocated hip – One step test – On
abduction of hip, relocation of a dislocated hip occurs
 Allis/Galeazzi sign – done in unilateral DDH – Flex both hips and
knees – At side of DDH, knees will be at a lower level

Sloping acetabulum & a break in Shenton's line

 Delayed appearance of the ossification centre of the head of
the femur.
Lateral and upward displacement of the ossification centre
of the femoral head
– to a chieve reduction of the head into the
acetabulum, and maintain it until the hip becomes clinically
stable and a 'round' acetabulum covers the head.
:
a) Closed manipulation under general anaesthesia.
b) Traction followed by closed manipulation {abduct
the hip}
c) Open reduction is indicated if closed reduction fails.

: A frog leg or Bachelor's cast

: Some form of splint such as Von Rosen's splint
: for older chldren
a) Salter's osteotomy: This is an osteotomy of the iliac bone,
above the acetabulum.
b) Chiari's pelvic displacement osteotomy: The iliac bone is
divided almost transversely immediately above the
acetabulum, and the lower fragment (bearing the
acetabulum) is displaced medially.
c) Pemberton's pericapsular osteotomy: A curved osteotomy
is made. The roof of the acetabulum is deflected
downwards over the femoral head, with the fulcrum at the triradiate cartilage of the acetabulum.

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1. Gait [10]
Ans.
Normal gait: In normal walking, each leg goes
through a stance phase and a swing phase
alternately. The rhythmic repetition of such
cycles provides grace to the gait.

Abnormal gait: There are number of reasons

for abnormality of gait. Some of the typical abnormal gaits are as follows:
 Neuromuscular Disorders

1. Spina bifida Aperta [14]

a. Meningomyelocele [16]
Ans. Failure of fusion of vertebral arches gives rise to spina bifida
Spina bifida Aperta is developmental defect which not only involves vertebral arches but also soft
tissues, skin and meninges.
Commonest site: The dorso-lumbar spine
There is a variable structural defect of closure of the embryonal neural tube giving
rise to the following:
a) Meningocele – protrusion of meninges through a defect in the neural arch.
b) Meningomyelocele – protrusion of the meninges along with some
neural elements (normally developed spinal cord or cauda equina).
c) Syringomyelocele – central canal of the cord is dilated
(syringomyelia), and the cord lies within the protruded meningeal
sac together with the nerves arising from it.
d) Myelocele: An elliptical raw surface, representing the ununited groove is seen. At
the upper end of this surface opens the central canal through
which CSF may be seen leaking.
Treatment
 Treat the basic defect i.e., spina bifida
 Orthopaedic treatment to prevent and correct the deformities, and to use the residual motor
power in the best possible way
 Urological treatment for bladder incontinence.
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1) Post-Polio Residual paralysis of left lower limb in a child of 12 years and its Mx [11]
Ans.
 PRPP may result in wasting, weakness, and deformities
 The common deformity at the hip is flexion-abduction-external rotation. F Ab Er
 At the knee, flexion deformity is common; in severe cases triple deformity comprising of flexion,
posterior subluxation and external rotation occurs.
 At the foot, equino-varus deformity is the commonest
 Management:
 Evaluate the deformities and muscle weakness
 Prevention or correction of deformities – splint the paralysed part; Operations for correcting the
deformities are:
 For hip deformity (flexion-abduction-external rotation): Soutters’ release
 For knee flexion deformity: Wilson’s release
 For Equinus deformity of the ankle: Tendoachilles lengthening
 For cavus deformity of the foot: Steindler’s release
 For a foot with severe muscle imbalance – tendon transfer operation
 Bone Tumors

1) Classify tumours of the bone. Describe the treatment of Ewing’s Sarcoma of the Humerus [10, 04]
a. Pathology and Radiological features of Ewing’s Sarcoma [14]
b. Benign bone tumours [06]
Ans.
Nomenclature and classification of bone tumours (WHO classification simplified)
• Benign - Osteoid osteoma, osteoma, Osteoblastoma
a) Bone forming
• Indeterminate - Aggressive osteoblastoma
tumours
• Malignant – Osteosarcoma
b) Cartilage • Benign - Osteochondroma (exostosis), Enchondroma (chondroma),
forming Chondromyxoid fibroma, Chondroblastoma
tumours • Malignant – Chondrosarcoma
• Benign GCT
c) Giant cell
• Indeterminate GCT
tumours (GCT)
• Malignant GCT
• Malignant - Ewing’s sarcoma
d) Marrow - Plasma cell tumour
tumours - Multiple myeloma
- Lymphoma
• Benign - Haemangioma
e) Vascular
- Glomangioma
tumours
• Malignant - Angiosarcoma
EWING’S SARCOMA
This is highly malignant tumour occurring between the
age of 10-20 years, sometimes up to 30 years.
Pathology:
 Bones affected: mainly in the femur and tibia (70%),
pelvis and calcaneum (30%)
 Site: The tumour may begin anywhere, but diaphysis
of the long bone is the most common site.
 Gross appearance: The tumour characteristically
involves a large area, or even the entire medullary cavity.
Radiological features: In a typical case, there is a lytic lesion in the
medullary zone of the midshaft of a long bone, with cortical destruction
and new bone formation in layers – onion-peel appearance.
Treatment:
• This is a highly radio-sensitive tumour, melts quickly but recurs.
• Control of local tumour by radiotherapy (6000 rads), and control of
metastasis by chemotherapy.
• Chemo­therapy consists of Vincristine, Cyclophos­phamide, and
Adriamycin in cycles
Prognosis: It is very poor – because in most cases, distant metastasis
has occurred by the time diagnosis is made
----------------------------------------------------------------------------------------------------------------------------------------
1. Osteoclastoma [21, 15, 12, 09, 06, 02]
a. Giant Cell tumor – commonly affected bones, location & X-Ray findings [19, 13, 11, 07, 04]
Ans.
Giant cell tumour (GCT) generally classified as benign; it tends to recur after local removal. The giant
cells were mistaken as osteoclasts in the past, hence the name osteoclastoma.
: Primitive stromal cells
Primitive osteoblast precursors cause proliferation & differentiation of osteoclast
precursors into mature osteoclasts  cause destructive resorption of bone matrix

The tumour is seen commonly in the age group of 20-40 years i.e, after epiphyseal fusion.
Bones affected: lower-end of the femur and upper-end of the tibia (around the knee)
The tumour is located at the epiphysis..
Common presenting complaints are swelling and vague pain.
EXAMINATION: Examination reveals a bony swelling with smooth surface, eccentrically located
at the end of the bone. There may be tenderness on firm palpation. A characteristic ‘egg-shell
crackling’ is often not elicited. The limb may be deformed if a pathological fracture has
occurred.
: Following are some of the characteristic
radiological features of this tumour:
A solitary, may be loculated, lytic lesion.
Eccentric location, often subchondral.
Expansion of the overlying cortex (expansile lesion).
‘Soap-bubble’ appearance – the tumour is
homogeneously lytic with trabeculae of the remnants of
bone traversing it, giving rise to a loculated appearance.
Excision of the tumour is the best treatment.
Excision with reconstruction by one of the following methods:
 Arthrodesis by the Turn-o-Plasty procedure. In this technique, the
required length of the tibia is split into 2 halves. One half is turned
upside down and fixed with the stump of the femur left after excising
the tumour.
 Arthrodesis by bridging the gap by double fibulae, one taken from
same extremity and the other from the opposite leg
 Arthroplasty: the tumour is excised, and an attempt is made to
reconstruct the joint in some way
----------------------------------------------------------------------------------------------------------------------------------------
2. Osteosarcoma & it’s Radiology [19, 06, 05]
Ans.
An osteosarcoma is defined as a malignant tumour of the mesenchymal cells, characterised by
formation of osteoid by the tumour cells.
Age at onset: These tumours occur between the ages of 15-25 years
Common sites of origin: In decreasing order of frequency these are: the lower-end of the femur;
upper-end of the tibia; and upper-end of the humerus.
Gross appearance of the tumour depends upon its dominant histo-morphology.
 An osteoblastic tumour is greyish white, hard, and has a gritty feeling when cut
 A chondroid type may appear opalescent and bluish grey
 A fibroblastic type has a more typical fish flesh sarcomatous appearance.
 Telangiectatic type may have large areas of tumour necrosis
Clinical features:
 Pain & swelling in the involved bone
 Pain is constant and boring, and becomes worse as the swelling increases in size.
 Examination: The swelling is warm and tender in the region of the metaphysis. Skin over the
swelling is shiny with prominent veins.
Radiological examination: X-ray shows the following features
 An area of irregular destruction in the metaphysis,
sometimes overshadowed by the new bone formation.
There is new bone formation in the matrix of the tumour.
 Periosteal reaction: irregular, unlike in osteomyelitis where
it is smooth and in layers.
 Codman’s triangle: A triangular area of subperiosteal new
bone is seen at the tumour-host cortex junction at the ends
of the tumour.
 Sun-ray appearance: New bone is laid down along the blood
vessels within the tumour growing centrifugally, giving rise to a ‘sun-ray appearance’ on the X-ray.
Management:
Confirmation of the diagnosis – via biopsy – tumour new bone formation is patho­gnomonic of
osteosarcoma.
Evaluation of spread of tumour: Lung is the earliest site for metastasis  Do a chest X-ray
Treatment of the tumour:
 Local control by surgical ablation; amputation.
 Adjuvant chemotherapy, immunotherapy etc. – to control distant metastasis – The drugs used
are high dose Methotrexate, Citrovorum factor, Endoxan, and sometimes Cisplatinum.
Follow up: The patient is checked up every 6-8 week for any evidence of recurrence.
----------------------------------------------------------------------------------------------------------------------------------------
3. Osteoid Osteoma [15]
Ans. It is the commonest true benign tumour of the bone.
Pathologically, it consists of a nidus of tangled arrays of partially mineralised osteoid trabeculae
surrounded by dense sclerotic bone.
:
Seen commonly between the ages of 5-25 years.
Bones affected: Tibia (MC)
Site: diaphysis of long bones.
Nagging pain, worst at night, and is relieved by salicylates.
There are minimal or no clinical signs, except for mild tenderness at the site of the lesion, and a
palpable swelling if it is a superficial lesion.
: confirmed on X-ray or CT zone of sclerosis surrounding a radiolucent nidus.
: Complete excision of the nidus along with the sclerotic bone is done.
is good. It is not a pre-malignant condition.
----------------------------------------------------------------------------------------------------------------------------------------
4. Plasmacytoma [14, 03]
Ans.
Plasmacytoma is a malignant neoplasm derived from plasma cells.
: The neoplasm characteristically affects flat bones i.e., the pelvis, vertebrae, skull, and
ribs. It may occur as a solitary lesion (plasmacytoma), multiple lesion (multiple myeloma).
:
 The tumour affects adults above 40 years of age. Men>women.
 Increasingly severe pain in the lumbar and thoracic spine.
 Pathological fractures, especially of the vertebrae and ribs.
 The patient is weak, and will have loss of weight.
 Neurological symptoms may result if the tumour presses on the spinal cord or it’s nerves
are as follows
 Multiple punched out lesions in the skull and other flat bones.
 Pathological wedge collapse of the vertebra.
 Diffuse, severe rarefaction of bones.
 Erosions of the borders of the ribs.
: control the tumour by chemotherapy & splintage to diseased part by POP, brace etc.
 Chemotherapy: Melphalan is the DOC. It is given in combination with Vincristine, Prednisolone,
and sometimes Cyclophosphamide. The cycles are repeated every 3-4 weeks for 6-12 cycles
 Radiotherapy helps in cases with neurological compression
----------------------------------------------------------------------------------------------------------------------------------------
5. Exostoses [13, 07, 02]
Ans.
Diaphyseal aclasis (Multiple exostosis)
:
This is a condition characterised by multiple, cartilage-capped
bony outgrowths from the metaphysis of long bones, and some
from flat bones.
It is inherited as an autosomal dominant disorder.
The basic defect is that of remodelling.
The columns of cartilage at the epiphyseal plate grow rapidly
and sideways due to poor remodelling forces.
: X-rays typically show a ‘trumpet-shaped’
metaphysis and bony projections from it.
: The problem is of dwarfism, pressure effects of the exostosis, deformities, and a
tendency of the exostosis to undergo malignant change.
: Since, it is impractical to excise all the exostosis, the one causing symptoms is excised.
----------------------------------------------------------------------------------------------------------------------------------------
6. Chondrosarcoma [11]
Ans.
This is a malignant bone tumour arising from cartilage cells.
It may arise in normal bone (primary chondrosarcoma), or in a pre-existing cartilaginous tumour such
as enchondroma (secondary chondrosarcoma).
: It is common in flat bones such as scapula, pelvis and ribs.
: It occurs commonly in adults between 30-60 years of age.
 pain and swelling, often of long duration
 The tumour has a wide spectrum of aggressiveness.
 Metastasis occurs through the blood vessels, commonly to the
lungs.
shows erosion of the cortex and bone destruction. The
tumour matrix may have mottled calcification, typical of a
cartilaginous tumour.
confirms diagnosis
depends upon the behaviour of the tumour.
 Amputation is necessary for most tumours.
 In some low grade tumours, after proper assessment, wide
resection of the tumour is done (limb saving surgery).
 Role of chemotherapy and radiotherapy is doubtful.

----------------------------------------------------------------------------------------------------------------------------------------

1. Aneurysmal bone cyst [08]

Ans.
This is a benign bone lesion which consists of a blood-filled space enclosed in a shell, ballooning up
the overlying cortex.
Common sites are the long bones, usually at their ends {metaphysis} in the Age 10-40 years.
Clinical Features: A gradually increasing swelling with little pain & pathological fracture
Radiological Features: Eccentric well-defined radiolucent area with Expansion of the overlying
cortex {Distending lesion, ‘ballooning’ the bone}
Treatment is by curettage and bone grafting
----------------------------------------------------------------------------------------------------------------------------------------
2. Brown Tumour [07]
Ans.
Seen in Primary Hyperparathyroidism {refer 2nd SQ – Metabolic Bone Disease}
 Metabolic Bone Disease

1. Nutritional Rickets [16, 10, 07]

a. C/F of Rickets [19]
Ans.
Rickets is a disease of the growth plate characterized by deficient mineralization
As it is a disorder of growing bones, it invariably presents by 18 months of age
:
Vitamin D deficiency – poor sunlight exposure, inadequate dietary intake, deficient
hydroxylation in cirrhosis & renal failure.
Deficient Vitamin D action – seen in Vitamin D resistant ricket
Hypophosphatemia – seen in renal tubular acidosis, Antacids etc.
Defective mineralisation – Ex: osteogenesis imperfecta, fibrogenesis imperfecta etc.
:

:
 Most are diagnosed by classical radiological
features— cupping, splaying and flaying of the
metaphysis
 Diagnosis is supported by a detailed history, an
extensive clinical examination and laboratory test
results {Low 25(OH)D3; ALP}
:�

----------------------------------------------------------------------------------------------------------------------------------------
2. Hyperparathyroidism [05]
Ans.
Hyperfunctioning of parathyroid gland with elevated PTH levels.
Types:
1) Primary Hyperparathyroidism
2) Secondary Hyperparathyroidism
: “An autonomous overproduction of PTH is seen.” MC cause of
asymptomatic hypercalcemia.
 : Adenoma (MC); Primary hyperplasia; Carcinoma
 : Elderly Female
It can be Sporadic (MC) or Familial
Genetic alterations with sporadic adenomas:
1) Cyclin D1 gene inversions leading to overexpression of cyclin D1
2) Mutations involving MEN1 tumor suppressor gene
Familial parathyroid adenomas; They are seen with MEN-1 & MEN-2A, caused by germline
mutations of MEN1 & RET.
Clinical Presentations: Asymptomatic or can exhibit the following symptomatic primary
hyperparathyroidism:
 Bone: Osteoporosis & osteitis fibrosa cystica leading to fractures.
 GIT: Constipation, nausea, peptic ulcers, & pancreatitis
 Renal: Nephrolithiasis & chronic renal insufficiency
 CNS: Depression, lethargy, & seizures
 Neuromuscular: Weakness & fatigue
 Cardiac: Aortic or mitral valve calcifications
Inv.: Elevated PTH levels, Hypercalcemia, hypophosphatemia, increased urinary excretion of both
calcium & phosphate.
: “Compensatory overactivity of the parathyroid glands due to
chronic hypocalcemia.”
 Causes: Renal failure (MC), inadequate intake of calcium, Vit. D deficiency, & steatorrhea.
 Clinical Presentations:
1) Features of chronic renal failure
2) Milder skeletal abnormalities
3) Ischemic damage to tissues (calciphylaxis)
Treat the cause {Ex: surgical excision of the hormone secreting tissue}.
 Orthopedic treatment – directed towards adequate protection of the softened bones from all
deforming stress and strain.
 Urology treatment – directed towards the removal of calculi and maintenance of renal functions.
----------------------------------------------------------------------------------------------------------------------------------------
3. Osteoporosis [03]
Ans.
Osteoporosis is by far the commonest metabolic bone disease
which is occurs when the rate of bone resorption exceeds the rate
of bone formation  decrease in bone mass.
�

 Osteoporosis is an asymptomatic disorder unless complications

(predominantly fractures) occur.
 Dorso-lumbar spine is the most frequent site
 Others are: Colles' fracture & fracture of the neck of femur.

 Loss of vertical height of a vertebra due to collapse.

 Cod fish appearance: The disc bulges into the adjacent vertebral bodies disc becomes biconvex.
 Ground glass appearance of the bones.
 Singh's index: osteoporosis is graded into 6 grades.
 Metacarpal index and vertebral index are other methods of quantification of osteoporosis.

Biochemistry: Serum calcium, phosphates, ALP & Total plasma proteins and plasma albumin
Densitometry – to quantify osteoporosis.; 2 types – ultrasound based and X-ray based. DEXA scan
is an X-ray based bone densitometry, and is the gold standard in the quantification of bone mass.
Neutron activation analysis: In this method, calcium in the bone is activated by neutron bombing,
and its activity measured.
Bone biopsy.
treat the cause, alleviate the pain & prevent fractures
:
High protein diet for elderly patients
Calcium supplementation.
Vitamin D – to increase calcium absorption from the gut
Androgens – they have an anabolic effect on the protein matrix of bone
Estrogens – they halt the progressive loss of bone mass in postmenopausal osteoporosis.
Calcitonin – helps in building up the bone mass and also acts as an analgesic.
Teriparatide: Anabolic agent which  osteoblastic new bone formation.
Denosumab, Strontium – Antiresorptive agents.
:
Exercises: Weight bearing is a major stimulus to bone formation.
Bracing: Prophylactic bracing of the spine by using an ASH brace or Taylor brace may be useful
in prevention of pathological fractures in a severely osteoporotic spine.
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1. Gout & Pseudo Gout [14]

a. Gouty Arthritis [10]
Ans.
 Amputation & Prosthetics

1. Below knee amputation [20]

a. Mention 4 indications for amputation [15, 14]
Ans.
Amputation is a procedure where a part of the limb is
removed through one or more bones
Below knee amputation – aka transtibial amputation
 Indications: �
 PTB (Patellar Tendon Bearing) prosthesis is used for Below-
knee amputations

----------------------------------------------------------------------------------------------------------------------------------------
2. Complications of major amputation [02]
Ans.
a) : It results in delayed wound healing and infection. It should be aspirated and a
pressure bandage given.
b) Infection – occurs if there is a PVD, diabetes or a haematoma.
c) Skin flap necrosis – it indicates insufficient circulation of the skin flap.
d) – occurs due to improper positioning of the amputation stump, leading to
contractures.
e) : A neuroma always forms at the end of a cut nerve. If it is bound down to the scar
because of adhesions, it becomes painful.
f) Phantom sensation – a sensation as if the amputated part is still present. This gradually diminishes
with time. Phantom pain is the awareness of pain in the amputated limb.
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1. Austin Moore prosthesis [10]

Ans.
Used in fracture neck of the femur for replacement of femoral head in elderly
persons
The prosthesis has a head with a small neck and a stem.
There is a small hole at the top of the stem for the hook of the extractor, used while
removing the prosthesis.
The stem has 2 fenestrations in its middle, through which the bone supposedly grows and helps in
fixation of the prosthesis
 Prolapsed Intervertebral Disc

1) Discuss Prolapse of lumbar intervertebral Disc at L4-L5 level, it’s Mx & complications [10]
a. Intervertebral disk prolapse – pathology and clinical features [17, 01]
Ans.
 The term 'prolapsed disc' means the protrusion or extrusion of the nucleus pulposus through a rent
in the annulus fibrosus.
 The commonest level of disc prolapse is between L4-L5 in the lumbar spine.
 The sequence of changes in the disc, which ultimately lead to it prolapse are the following:

 The site of exit of the nucleus is usually posterolateral

 CLINICAL FEATURES –
 low backache – usually made worse by exertion,
forward bending, sitting or standing in one position
for a long time. It is relieved by rest
 Sciatic pain: The pain radiates to the gluteal region,
the back of the thigh and leg
 Paraesthesia’s in the dermatomes of the affected
nerve root
 O/E:
 The patient is unable to bend forwards; any such attempt initiates severe
muscle spasm in the paraspinal muscles
 Diffuse tenderness in the lumbo-sacral region
 Tests: Straight leg raising test (SLRT); Lasegue test
 Investigations: MRI Scan is the investigation of choice. Other options:
• Myelography
• Root cut off sign – appears on the X-ray, as an abrupt
blunting of the dye column filling the root sheath.
• CT scan – the posterior border of a disc appears flat or
convex.
 Complications: Compression of nerve root; Cauda equina
syndrome & degenerative arthritis of the vertebra.
 TREATMENT:
Conservative Treatment
Rest on a hard bed
Drugs – Analgesics and muscle relaxants.
 Physiotherapy – hot fomentation, gentle arching exercises, etc.
Others: These consist of lumbar traction, transcutaneous electrical nerve stimulation (TENS) etc.
Operative Treatment
– excise the ligamentum flavum bridging the two adjacent laminae
: In addition to fenestration, a
hole is made in the lamina for wider
exposure.
: The whole of the lamina
on one side is removed.
: The laminae on both sides,
with the spinous process, are removed. Such a wide exposure is required for a big, central disc
producing cauda equina syndrome
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1. Spondylolisthesis [13, 11, 09]

Ans.
Spondylolisthesis is forward displacement of a vertebra over the one below it. It commonly occurs
between L4-L5 and between L5-S1.
Clinical features:
Backache, with or without sciatica.
Symptoms become worse on standing or walking.
On examination, there is often a visible or palpable 'step'
above the sacral crest due to the forward displacement of the
spinal column. There may be lumbar lordosis & evidence of
stretching of the sciatic nerve found by the straight leg raising test (SLRT).
X-ray examination:
Anterior displacement of one vertebra over other can be seen on a lateral view of the spine.
An oblique view of the spine may show defect in the pars interarticularis.
- In this view, in a normal vertebra, the pars interarticularis looks like a 'Scottish dog'.
- In Spondylolisthesis, vertebra slips over other giving “beheaded Scottish terrier” sign
TREATMENT
1. Conservative methods – rest & external support to the affected segment + flexion exercises.
2. Operative methods – decompression of the compressed nerves if any, followed by fusion of the
affected segments of the spine (intertransverse fusion).
Use of internal fixation devices like pedicular screws and rods can help in early mobilisation of
the patient.
 Spinal Injuries

1. Write mechanism of fracture spine, complications and management [04]

Ans.
MODE OF INJURY - fall from height, e.g., a fall
from a tree, RTA, fall of a heavy object on the
back e.g., fall of a rock onto the back of a miner,
sports injuries etc.

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1) Whiplash injury [2000]

Ans.
It is a Cervical spine injury where sudden flexion followed by hyperextension takes place. There is no
fracture of vertebral column.
Causes: RTA, Boxing and karate
Clinical features:
• Pain in neck, shoulder and back.
• Headache, dizziness, paresthesias, paralysis
Treatment: common cervical collar or cervical orthosis
 Arthritis & Related Disorders

1. Rheumatoid arthritis [20, 11, 06]

Ans.
Rheumatoid Arthritis is a systemic autoimmune disease characterised by inflammatory polyarthritis,
which affects peripheral joints, especially the small joints of the hands & feet

RA might be a manifestation of the response to an infectious agent (Mycoplasma, EBV, CMV,

parvovirus, and rubella virus) in a genetically susceptible host.
Most patients with RA are HLA-DR4 +ve.
Risk factors: Female gender and cigarette smoking

RA is characterized by chronic inflammation, granuloma formation and joint destruction.

Lymphocytes (CD4+ T cells), plasma cells and macrophages infiltrate the synovial membrane 
Swelling and congestion  release of cytokinesB cells differentiate into plasma cells
antibodies against the Fe fragment of IgG which is termed as the rheumatoid factor.
Inflammation of synovium synovial hypertrophy and effusion of synovial fluid into the joint
space  joint swelling.
Inflammatory granulation tissue (pannus) forms  spreads around & damage the articular cartilage
 fibrous or bony ankylosis.
Muscles adjacent to inflamed joints atrophy and there may be focal infiltration with lymphocytes.
Subcutaneous nodules consist of a central area of fibrinoid necrosis surrounded by radially
arranged (palisade) mononuclear cells with strands of collagen.
Rheumatoid vasculitis involves medium and small arteries and venules, with infiltration by
lymphocytes.
Age of onset & Sex: 20 - 50 y/o females.
Typical presentation: An acute, symmetrical polyarthritis: Pain & stiffness in multiple joints
(at least 4), particularly in the morning, mark the
beginning of the disease. This may be followed by • MP joints of hand
frank symptoms of articular inflammation. Joints Common • PIP joints of fingers
affected in Rheumatoid arthritis are: � • Wrists, knees, elbows, ankles
The onset may be with fever or visceral Less
manifestations like: pneumonitis, rheumatoid Hip joint & TMJ
common
nodules etc. • Atlanto-axial joint
Uncommon
Examination – reveals • Facet joints of cervical spine
Ulnar drift of the hand
swollen boggy joints. Boutonniere deformity
Hand
Joints of the hand Swan neck deformity
show typical Elbow Flexion deformity
deformities. � Early - flexion deformity
Limited ROM Knee
Late - triple* subluxation
Ankle Equinus deformity
Foot Hallux valgus, Hammer toe
There may be fever, rash & signs suggestive of systemic vasculitis.
The rash in rheumatoid arthritis is typically non-pruritic and maculo-papular on the face, trunk and
extremities.
Extra-articular manifestatiosn �

Investigations: �
The goals of treatment are: (1) Relief of pain, (2)
Reduction of inflammation, (3) Protection of articular
structures, (4) Maintenance of function, and (5) Control
of systemic involvement.

Analgesics – to pain – Ex: Acetaminophen (PCM), &

NSAIDs (diclofenac, ibuprofen, aceclofenac)
DMARDs (disease-modifying antirheumatic drugs) – to
 joint damage – Ex: hydroxychloroquine (200-400 mg daily),
methotrexate (7.5-25 mg per week), sulfasalazine,
leflunomide, gold salts etc.
Steroids – to inflammation – Ex: prednisolone, triamcinolone, etc.
Immunosuppressive agents - used as 3rd line drugs – Ex: azathioprine and cyclophosphamide
Biological response modifiers
 Etanercept (subcut. Inj.)– TNF receptor blocker – used in many forms of inflammatory arthritis
like RA, psoriatic arthritis, and ankylosing spondylitis.
 Infliximab – antibody against TNF - given as IV infusion every six weeks
 Rituximab – anti-CD20 antibody.
 Anakinra – interleukin-I receptor antagonist

Patient education and counselling – Explain about the chronic nature of disease, the need for long-
term therapy, the side effects of drugs & the need for follow-up stressed.
 Rest – during acute arthritis and during flare ups.
Exercise – to improve joint mobility, contractures, and muscle atrophy.
Physiotherapy – application of heat or cold to relieve pain or stiffness; ultrasound to tenosynovitis,
passive and active exercises to improve and maintain joint motion range.
– indicated when medical therapy fails
 Synovectomy of the wrist or finger tendon sheaths – for pain relief or to prevent tendon rupture.
 Osteotomy, arthrodesis or arthroplasties – done in advanced disease.
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2. Charcot's joint [05]
Ans. Foot drop
 It is a Neuropathic arthropathy where repeated strain on a joint due to loss of sensations leads to
severe degeneration
 Clinically, the joint manifests as painless effusion, deformity or instability
 The X-ray changes are those of severe osteoarthritis but without much clinical findings like pain,
muscle spasm etc.
 Treatment is difficult.
Bracing is usually advised for some joints.
Others require Fusion of the joint
 Degenerative Disorders

1. Osteoarthritis – etiopath, C/F, inv. & Tt [13, 04]

a. Osteoarthritis of knee joint [07, 2000]
Ans. Osteoarthritis (OA) is a degenerative joint disease. Commonly it is thought to be wear and tear of
joints as one ages.

Investigations
:
 Narrowing of joint space.
 Subchondral sclerosis – dense bone under the articular surface
 Subchondral cysts, Osteophyte formation, Loose bodies & Deformity of the joint
– to detect an underlying cause. Ex:
 Serological tests and ESR to rule out rheumatoid arthritis
 Serum uric acid to rule out gout
Treatment
To delay the occurrence of the disease, if the disease has not begun yet – Ex: Weight reduction, in
an obese patient
To stall progress of the disease and relieve symptoms – Avoid stress & strain to the affected joint;
Local heat; Analgesics & Chondroprotective agents {Glucosamine and Chondroitin sulphate}; Inj.
Sodium Hyaluronan into the joint space
To rehabilitate the patients with disability via surgery – Osteotomy; Joint replacement,
Arthroscopic procedures etc.
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1) Cervical Spondylosis [05]

Ans.
This is a degenerative condition of the cervical spine. The pathology lies in the intervertebral discs
Occurs in persons susceptible to neck strain because of keeping the neck constantly in one position
while reading, writing etc.
: Occipital headache, Pain and stiffness in neck
 Patient may present with pain radiating to the shoulder or paraesthesia
 Patient may present with an episode of giddiness because of vertebro-basilar syndrome.
– X-ray of cervical spine – reveals Narrowing of intervertebral disc spaces
 : aimed at assisting the natural resolution of the temporarily inflamed soft tissues –
Analgesics; Hot fomentation; Rest to the neck in a cervical collar;
Traction to the neck if there is stiffness.
Anti-emetics, if there is giddiness
:
 Proper neck posture: Patient must avoid situations where he has to keep his neck in one position
for a long time. Only a thin pillow should be used at night
 Neck muscle exercises: These help in improving the neck posture
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1. Lumbar Spondylosis [14]

Ans.
This is a degenerative disorder of the lumbar spine which begins in the inter­vertebral joints
Clinical Features: low backache, initially worst during activity, feeling of ‘a catch’ while getting up
from a sitting position; Pain may radiate down the limb up to the calf (sciatica) because of irritation
of one of the nerve roots.
Good AP and lateral views of the lumbo-sacral spine is needed for the diagnosis
Treatment: {same as cervical spondylosis}
 Affections of Soft Tissue

1. Carpel tunnel syndrome [21, 19, 16, 03, 02]

Ans.
This is a syndrome characterised by the compression of
the median nerve as it passes beneath the flexor
retinaculum
Causes: Any space occupying lesion of carpal tunnel + �
Clinical features: The patient is generally a middle-aged woman
complaining of tingling, numbness or discomfort in the thumb and radial
one and a half fingers i.e., in the median nerve distribution.
 On examination, features of low median nerve compression are found.
 Nerve conduction studies show delayed or absent conduction of
impulses in the median nerve across the wrist.
Treatment is by dividing the flexor retinaculum, and thus decompressing the nerve
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2. Dupuytren’s contracture [09, 04]
Ans.

 This is a condition characterised by a flexion deformity of one or more fingers due to a thickening
and shortening of the palmar aponeurosis.
 The cause is unknown, but risk factors are: genetics, cirrhosis, sodium hydantoin etc.

 In early stages, thickening of the palmar aponeurosis is felt at the bases of ring and little fingers.
 Later, a flexion deformity of the fingers develops.
 In Dupuytren's contracture only the MP and PIP joints are flexed

 Mild contracture does not need any treatment.

 If the deformity is significant and hampers the activity of the patient, excision of the palmar
aponeurosis (subtotal excision) may be required.
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1. Plantar fasciitis [16]

Ans.
Plantar fasciitis occurs as a result of inflammation of the plantar aponeurosis at its attachment on
the tuberosity of the calcaneum.
: This is a common cause of pain in the heel
 The pain is worst in the early morning, and often improves with activity.
 On examination, there is marked tenderness over the medial aspect of the calcaneal tuberosity,
at the site of attachment of the plantar fascia
: Analgesics + use of a heel pad and local induction of steroids brings relief in most
cases.
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2. Ganglion [15, 09]
Ans.
It is the commonest cystic swelling on the dorsum of the wrist.
Etiology: It results from mucoid degeneration of the tendon sheath or the joint capsule.
Clinical Features: Ordinarily, there are no symptoms other than the swelling itself. Sometimes, a
mild discomfort or pain is experienced.
Management: Aspiration of the cyst + injection of hylase given. If the cyst recurs, excision may be
required
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3. Tenosynovitis [09]
a. Compound palmar ganglion [04]
Ans.
Inflammation of the thin synovial lining of a tendon sheath is
termed tenosynovitis.
Pain and swelling at the affected joint
:
- arise from mechanical irritation –commonly seen in the tendons of the
hand. Treatment is by rest, analgesics, ultrasonic therapy. Some cases need local hydrocortisone
infiltration
– occurs due to bacterial Infection by pyogenic or tubercular bacteria.
Pyogenic infection is common in the flexor tendons of the hand.
TB tenosynovitis of flexor tendons at wrist is referred to as Compound palmar ganglion
 Miscellaneous

1. Role of physiotherapy in orthopaedic problems [15]

Ans.

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2. MRI in Orthopaedics [14]
Ans.
MRI is a non-invasive procedure which helps to visualise the structures
T1 weighed images – sharp, well-defined – provide good anatomic detail
T2 weighed images used for evaluation of pathologic processes
:
MRI SPINE – to evaluate Inter Vertebral Disc, spinal tumours & spinal trauma
MRI knee – to evaluate Meniscal injuries, ACL & PCL injuries
MRI Hip – to detect Occult femoral fractures, osteonecrosis etc.
MRI shoulder – to evaluate Rotator cuff tears, Impingement syndromes, occult frctures etc.
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3. Torticollis & it’s causes [12, 03]
Ans.
Torticollis (Wry neck) is a deformity of the neck where the
head and neck are turned and twisted to one side.
It may be permanent, temporary, or spasmodic.
Spasmodic torticollis is the commonest.
Congenital Torticollis (Infantile torticollis, Sterno-mastoid
tumour) – occurs due to ischaemic necrosis of SCM at birth
in breech presentation
Congenital Torticollis is a common cause of permanent torticollis
:
 Ischemic lump in SCM
CIRNOO
 the SCM is prominent on the side the head tilts, and becomes more prominent on trying to
passively correct the head tilt.
 Facial asymmetry develops in cases who present later in life.
 Radiological examination is normal, and is done to rule out an underlying bone defect such as
scoliosis.
:
Passive stretching and splinting – to halt the progress in mild deformities in younger children  .
Surgical release of the contracted SCM – in severe deformities, especially in older children.
Following surgery, the neck is maintained in the corrected position in a Callot's cast
 Most often, torticollis is secondary to pain and reflex muscle spasm and recovers once the
inflammatory process subsides.
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4. Osteogenesis imperfecta [10, 05]
Ans.
This condition is characterised by tendency for frequent
fractures because of weak and brittle bones.
: It results from defective collagen synthesis, and thus affects other collagen containing
soft tissues such as the skin, sclera, teeth, ligaments etc., as well.
 The disease is commonly inherited as an autosomal dominant disorder, but a severe variant is
known to occur where the inheritance is autosomal recessive.
: Typically, the patient has a tendency for frequent fractures, usually with
minimal trauma.
 Associated features are blue sclera, joint laxity and otosclerosis in adulthood.
:
No cure – only symptomatic management; Gene therapy can be tried
Patients with the severe type do not survive beyond a few years, but those with the milder
disease live their full life interrupted by frequent fractures.
The fractures unite normally but deformities secondary to malunion or joint contractures may
occur.
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5. Coxa Vara [08, 03]
a. Congenital coxa vara [13]
Ans.
Coxa vara is a term used to describe a reduced angle between
the neck and shaft of the femur.
It may be congenital or acquired.
Infantile Coxa Vara result from some unknown growth anomaly
at the upper femoral epiphysis.
Clinical presentation: painless limp in a child who has just
started walking.
 In severe cases, shortening of the leg may be obvious.
 On examination: abduction and internal rotation of the hip are limited and the leg is short.
X-rays will show a reduction in neck-shaft angle. The epiphyseal plate may be too vertical. There
may be a separate triangle of bone in the inferior portion of the metaphysis, called Fairbank's triangle
Treatment is by a sub­trochanteric corrective osteotomy.
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6. Hallux valgus [05]
Ans.
It is the lateral deviation of the great toe at the metatarso-phalangeal joint.
: rheumatoid arthritis, wearing pointed shoes with high heels,
idiopathic etc.
: Usually there are no symptoms. If symptoms are present,
surgical correction may be necessary.
:
(i) Osteotomy of neck of the 1st metatarsal (Mitchell's osteotomy);
 (ii) Excision of the metatarsal head (Mayo's operation); and
(iii) Excision of the base of the proximal phalanx (Keller's operation).
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7. Semilunar Cartilage [03]
Ans.
Semilunar Cartilages refer to Medial and Lateral Menisci found in Knee joint
These 2 crescent-shaped intra-articular discs are made up of fibrocartilage
They deepen the articular surfaces of the condyles of tibia,
and partially divide the knee joint cavity into the upper
(meniscofemoral) and lower (meniscotibial) compartments.
Flexion and extension of the knee take place in the upper
compartment, whereas the rotation of the knee occurs in
the lower compartment
Medial meniscus attaches to the medial collateral ligament &
is more prone to injury
Lateral meniscus attaches to the tendon popliteus muscle & is less prone to injury
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8. Arthroscopy [02]
Ans.
 Arthroscopy is a technique of surgery on the joints in which tip of a thin (4 mm diameter) telescope
called arthroscope is introduced into a joint, and the inside of the joint examined
 Once the diagnosis is made, necessary correction can be done, there and then, by introducing
micro-instruments through another small skin puncture  referred to as arthroscopic surgery.
 This technique has revolutionised the treatment
of joint disorders

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1. Bone Scan [21]

Ans.

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2. Osgood Schlatter’s Disease [13, 04]
Ans.
 It is osteochondritis of tibial tubercle  pain & swelling at the tibial tubercle
 Seen in growing epiphyses of children and adolescents
 It’s a common cause of knee pain in growing adolescents
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3. Albright Syndrome [12]
Ans.
 It is a developmental abnormality in girls
 it is a triad of Polyostotic fibrous dysplasia, precocious puberty & cutaneous pigmentation
 Treatment: Testolactone (aromatase inhibitor) can be used as a medical management
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4. Bunnell’s stitch [12]
Ans.

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5. Heat therapy [11]
a. Ultrasonic therapy in orthopaedic practice [16, 05, 04]
b. Shortwave diathermy treatment [14, 11]
Ans.
Heat produces a soothing effect on many body aches by increasing the blood flow.
Depending upon the depth of penetration of the heat, it can be:
a) Surface heat - only the skin and subcutaneous tissues are heated – Ex: hot water bottle (rubber-
bottle); warm bath; hot soaks or compresses etc.
b) Deep heat - deeper structures are heated – Ex: shortwave diathermy, ultrasonic therapy,
microwave etc.
 —heat generated by a high frequency alternating current (frequency 27
mega cycles/second) using a short-wave diathermy emitter
 – these waves (a million cycles/second) are projected as a beam from a
transducer;
 When the waves strike the tissues, energy is converted into heat.
 It is most useful for localised tender fibrous nodules
Heat application is done for 15 to 20 minutes 2 or 3 times a day.
Heat must not be applied if there is underlying acute infection or neoplastic tissue.
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6. Petit' s triangle [05]
Ans.
Lumbar triangle of petit
Boundaries: Significance:
 Medial – latissimus dorsi muscle  Site for lumbar hernia
 Laterally – external  Symptom Joure-Rozanov: pain in petit’s triangle when
oblique muscle pressed – seen in acute appendicitis
 Below – iliac crest  Extra-peritoneal laparoscopic approach to adrenal
glands
----------------------------------------------------------------------------------------------------------------------------------------
7. Laser therapy [03]

Ans.